• Journal of the Semiconductor & Display Technology
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• v.21 no.4
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• pp.27-32
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• 2022

RISC-V is an open instruction set architecture (ISA) developed in 2010 at UC Berkeley, and active research is being conducted as a processor to compete with ARM. In this paper, we propose an SoC system including an RV32I ISA-based 32-bit 5-stage pipeline processor and AHB bus master. The proposed RISC-V processor supports 37 instructions, excluding FENCE, ECALL, and EBREAK instructions, out of a total of 40 instructions based on RV32I ISA. In addition, the RISC-V processor can be connected to peripheral devices such as BRAM, UART, and TIMER using the AHB-lite bus protocol through the proposed AHB bus master. The proposed SoC system was implemented in Arty A7-35T FPGA with 1,959 LUTs and 1,982 flip-flops. Furthermore, the proposed hardware has a maximum operating frequency of 50 MHz. In the Dhrystone benchmark, the proposed processor performance was confirmed to be 0.48 DMIPS.

• Journal of the Microelectronics and Packaging Society
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• v.13 no.2 s.39
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• pp.21-26
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• 2006

We developed a bonding at low temperature using fine pitch Sn and In bumps, and studied the reliability of the fine pitch In-Sn solder joints. The $30{\mu}m$ pitch Sn and In bumps were joined together at $120^{\circ}C$. A non conductive adhesive (NCA) was applied during solder joining. Thermal cycling test ($0^{\circ}C-100^{\circ}C$, 2 cycles/h) of up to 2000 cycles was carried out to evaluate the reliability of the solder joints. The bondability was evaluated by measuring the contact resistance (Rc) of the joints through the four point probe method. As the content of filler increased, the reliability improved in the solder joints during thermal cycling test because the contact resistance increased little. The filler redistributed the stress and strains from the thermal shock over the entire joint area.

• Journal of the Institute of Electronics and Information Engineers
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• v.53 no.7
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• pp.17-26
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• 2016

This work proposes a 12b 60MS/s 0.18um CMOS Flash-SAR ADC for various systems such as wireless communications and portable video processing systems. The proposed Flash-SAR ADC alleviates the weakness of a conventional SAR ADC that the operation speed proportionally increases with a resolution by deciding upper 4bits first with a high-speed flash ADC before deciding lower 9bits with a low-power SAR ADC. The proposed ADC removes a sampling-time mismatch by using the C-R DAC in the SAR ADC as the combined sampling network instead of a T/H circuit which restricts a high speed operation. An interpolation technique implemented in the flash ADC halves the required number of pre-amplifiers, while a switched-bias power reduction scheme minimizes the power consumption of the flash ADC during the SAR operation. The TSPC based D-flip flop in the SAR logic for high-speed operation reduces the propagation delay by 55% and the required number of transistors by half compared to the conventional static D-flip flop. The prototype ADC in a 0.18um CMOS demonstrates a measured DNL and INL within 1.33LSB and 1.90LSB, with a maximum SNDR and SFDR of 58.27dB and 69.29dB at 60MS/s, respectively. The ADC occupies an active die area of $0.54mm^2$ and consumes 5.4mW at a 1.8V supply.

• Journal of Life Science
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• v.30 no.8
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• pp.661-671
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• 2020

The resistance of cancer cells to anti-cancer drugs is the leading cause of chemotherapy failure. The clinical use of nonsteroidal anti-inflammatory drugs (NSAIDs) has been gradually extended to cancer treatment through combination with anti-cancer drugs. In the current study, we investigated whether NSAIDs including celecoxib (CCB), 2,5-dimethyl celecoxib (DMC), and ibuprofen (IBU) could enhance the cytotoxic effects of imatinib and TNF-related apoptosis inducing ligand (TRAIL) on human cancer cells. We found that the NSAIDs potentiated TRAIL and imatinib cytotoxicity against human hepatocellular carcinoma (HCC) cell lines SNU-354, SNU-423, SNU-449, and SNU-475/TR and against leukemic K562 cells with high level of CD44 (CD44^highK562), respectively. More specifically, CCB induced endoplasmic reticulum stress via up-regulation of ATF4/CHOP which is associated with the induction of autophagy against HCC and CD44^high K562 cells. NSAID-induced autophagic activity accelerated TRAIL cytotoxicity of HCC cells through up- and down-regulation of DR5 and c-FLIP, respectively. The NSAIDs also potentiated imatinib-induced cytotoxicity and apoptosis through down-regulation of markers in CD44^highK562 cells that express a stemness phenotype. Our results suggest that the ability of NSAIDs to induce autophagy could enhance the cytotoxicity of TRAIL and imatinib, leading to a reverse resistance to these drugs in the cancer cells. In conclusion, NSAIDs in combination with low-dose TRAIL or imatinib may constitute a novel clinical strategy that maximizes therapeutic efficacy of each drug and effectively reduces the toxic side effects.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.10
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• pp.6115-6120
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• 2013

Introduction: Some non-small cell lung cancer (NSCLC) tumor cells are insensitive to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) -based therapy. This study was conducted to examine the effect of embelin on the sensitivity of the A549 NSCLC cell line to TRAIL receptor2 (TRAILR2) monoclonal antibodies and to investigate the potential mechanisms. Materials and Methods: A549 cells were treated with embelin, TRAILR2 mAb or a combination of both. Cell viability was measured using ATPlite assay and apoptosis rates were determined by flow cytometry with AnnexinV-FITC and propidium iodide staining, with the expression levels of proteins analyzed by Western blotting. Results: The cell survival rate of separate treatments with 100 ng/ml TRAILR2 antibody or 25 uM embelin were $81.5{\pm}1.57%$ and $61.7{\pm}2.84%$, respectively. Their combined use markedly decreased cell viability in A549 cells to $28.1{\pm}1.97%$ (P<0.05). The general caspase inhibitor Z-VAD-FMK could inhibit the embelin-enhanced sensitivity of A549 cells to TRAILR2 mAb ($75.97{\pm}3.17%$)(P<0.05). Both flow cytometry and cell morphological analysis showed that embelin was able to increase TRAIL-induced apoptosis in A549 cells. Combined treatment with embelin and TRAILR2 mAb augmented the activation of initiator caspases and effector caspase. In addition, A549 cells showed increasing levels of TRAILR2 protein and decreasing levels of Bcl-2, survivin and c-FLIP following the treatment with embelin+TRAILR2 mAb. Conclusions: Embelin could enhance TRAIL-induced apoptosis in A549 cells. The synergistic effect of the combination treatment might be due to modulation of multiple components in the TRAIL receptor-mediated apoptotic signaling pathway, including TRAILR2, XIAP, survivin, Bcl-2 and c-FLIP.

• Journal of the Microelectronics and Packaging Society
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• v.12 no.4 s.37
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• pp.315-321
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• 2005

Chip-on-glass technology to attach IC chip directly on the glass substrate of flat panel display was studied by using induction heating body in AC magnetic field. With applying magnetic field of 230 Oe at 14 kHz, the temperature of an induction heating body made with Cu electrodeposited film of 5 mm${\times}$5 mm size and $600{\mu}m$ thickness reached to $250^{\circ}C$ within 60 seconds. However, the temperature of the glass substrate was maintained below $100^{\circ}C$ at a distance larger than 2 mm from the Cu induction heating body. COG bonding was successfully accomplished with reflow of Sn-3.5Ag solder bumps by applying magnetic field of 230 Oe at 14 kHz for 120 seconds to a Cu induction heating body of 5mm${\times}$5mm size and $600{\mu}m$ thickness.

• Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
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• 2008.06a
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• pp.158-158
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• 2008

모바일 정보통신기기를 중심으로 실장모듈의 초소형화, 고집적화로 인해 접속단자의 피치가 점점 미세화 됨에 따라 플립칩 본딩용 접착제에 함유되는 무기충전제인 실리카 필러의 크기도 미세화되고 있다. 본 연구에서는 NCP (non-conductive paste)의 실리카 필러의 크기가 COB(chip-on-board) 플립칩 패키지의 신뢰성에 미치는 영향을 조사하였다. 실험에 사용된 실리카 필러는 Fused silica 3 종과 Fumed silica 3종이며 response surface 실험계획법에 따라 혼합하여 최적의 혼합비를 정하였다. 테스트베드로 사용된 실리콘 다이는 투께 $700{\mu}m$, 면적 5.2$\times$7.2mm로 $50\times50{\mu}m$ 크기의 Au 도금범프를 $100{\mu}m$ 피치, peripheral 방식으로 형성시켰으며, 기판은 패드를 Sn으로 finish 하였다. 기판을 플라즈마 전처리 후 Panasonic FCB-3 플립칩 본더를 이용하여 플립칩 본딩을 수행하였다. 패키지의 신뢰성 평가를 위해 $-40^{\circ}C{\sim}80^{\circ}C$의 열충격시험과 $85^{\circ}C$/85%R.H.의 고온고습시험을 수행하였으며 Die shear를 통한 접합 강도와 4-point probe를 통한 접속저항을 측정하였다.

• Herbal Formula Science
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• v.25 no.2
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• pp.145-154
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• 2017

Objectives : Bufalin is one of the bioactive component of 'Sum Su (蟾酥)', which is obtained from the skin and parotid venom gland of toad. Bufalin has been known to possess the inhibitory effects on cell proliferation and inducing apoptosis in various cancer cells. The tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) has concerned, because it can selectively induce apoptotic cell death in many types of malignant cells, while it is relatively non-toxic to normal cells. Here, we investigated whether bufalin can trigger TRAIL-induced apoptotic cell death in EJ human bladder cancer cells. Methods : Effects on the cell viability and apoptotic activity were quantified using MTT assay and flow cytometry analysis, respectively. To investigate the morphological change of nucleus, DAPI staining was performed. Protein expressions were measured by immunoblotting. Results : A combined treatment with bufalin (10 nM) and TRAIL (50 ng/ml) significantly promoted TRAIL-mediated growth inhibition and apoptosis in EJ cells. The apoptotic effects were associated with the up-regulation of death receptor proteins, and the down-regulation of cFLIP and XIAP. Moreover, our data showed that bufalin and TRAIL combination activated caspases and subsequently increased degradation of poly(ADP-ribose) polymerase. Conclusions : Taken altogether, the nontoxic doses of bufalin sensitized TRAIL-mediated apoptosis in EJ cells. Therefore, bufalin might be an effective therapeutic strategy for the safe treatment of TRAIL-resistant bladder cancers.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.6
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• pp.2129-2144
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• 2015

Programmed cell death (PCD) or apoptosis is a mechanism which is crucial for all multicellular organisms to control cell proliferation and maintain tissue homeostasis as well as eliminate harmful or unnecessary cells from an organism. Defects in the physiological mechanisms of apoptosis may contribute to different human diseases like cancer. Identification of the mechanisms of apoptosis and its effector proteins as well as the genes responsible for apoptosis has provided a new opportunity to discover and develop novel agents that can increase the sensitivity of cancer cells to undergo apoptosis or reset their apoptotic threshold. These novel targeted therapies include those targeting anti-apoptotic Bcl-2 family members, p53, the extrinsic pathway, FLICE-inhibitory protein (c-FLIP), inhibitor of apoptosis (IAP) proteins, and the caspases. In recent years a number of these novel agents have been assessed in preclinical and clinical trials. In this review, we introduce some of the key regulatory molecules that control the apoptotic pathways, extrinsic and intrinsic death receptors, discuss how defects in apoptotic pathways contribute to cancer, and list several agents being developed to target apoptosis.

• Journal of the Microelectronics and Packaging Society
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• v.5 no.1
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• pp.7-18
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• 1998

In the flip chip interconnection on organic substrates using eutectic Pb/Sn solder bumps highly reliable Under Bump Metallurgy (UBM) is required to maintain adhesion and solder wettability. Various UBM systems such as 1$\mu$m Al/0.2$\mu$m Pd/1$\mu$m Cu, laid under eutectic Pb/Sn solder were investigated with regard to their interfacial reactions and adhesion proper-ties. The effects of numbers of solder reflow and aging time on the growth of intermetallic compounds (IMCs) and on the solder ball shear strength were investigated. Good ball shear strength was obtained with 1$\mu$m Al/0.2$\mu$m Ti/5$\mu$m Cu and 1$\mu$m Al/0.2$\mu$m ni/1$\mu$m Cu even after 4 solder reflows or 7 day aging at 15$0^{\circ}C$. In contrast 1$\mu$m Al/0.2$\mu$m Ti/1$\mu$m Cu and 1$\mu$mAl/0.2$\mu$m Pd/1$\mu$m 쳐 show poor ball shear strength. The decrease of the shear strength was mainly due to the direct contact between solder and nonwettable metal such as Ti and Al resulting in a delamination. In this case thin 1$\mu$m Cu and 0.2$\mu$m Pd diffusion barrier layer were completely consumed by Cu-Sn and pd-Sn reaction.