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다중 시스템 클럭과 이종 코아를 가진 시스템 온 칩을 위한 연결선 지연 고장 테스트 제어기
장연실,이현빈,신현철,박성주,Jang Yeonsil,Lee Hyunbin,Shin Hyunchul,Park Sungju 대한전자공학회 2005 電子工學會論文誌-SD (Semiconductor and devices) Vol.42 No.5
본 논문은 SoC 상에서 정적인 고장 뿐 아니라 동적인 고장도 점검하고 진단할 수 있는 새로운 At-speed Interconnect Test Controller (ASITC)를 소개한다. SoC는 IEEE 1149.1과 P1500 래퍼의 코아들로 구성되고 다중 시스템 클럭에 의해 동작될 수 있으며, 이러한 복잡한 SoC를 테스트하기 위해 P1500 래퍼의 코아를 위한 인터페이스 모듈과 update부터 capture까지 1 시스템 클럭으로 연결선의 지연 고장을 점검할 수 있는 ASITC를 설계하였다. 제안한 ASITC는 FPGA로 구현하여 기능검증을 하였으며 기존의 방식에 비해 테스트 방법이 쉽고, 면적의 오버헤드가 적다는 장점이 있다. This paper introduces a new At-speed Interconnect Test Controller (ASITC) that can detect and diagnose dynamic as well as static defects in an SoC. SoC is comprised of IEEE 1149.1 and P1500 wrapped cores which can be operated by multiple system clocks. In other to test such a complicated SoC, we designed a interface module for P1500 wrapped cores and the ASITC that makes it possible to detect interconnect delay faults during 1 system clock from launching to capturing the transition signal. The ASITC proposed requires less area overhead than other approaches and the operation was verified through the FPGA implementation
대식세포주에서 인슐린이 $I{\kappa}B/NF-{\kappa}B$ 경로 활성화에 미치는 영향
이상민,장연실,이춘택,김영환,한성구,심영수,유철규,Lee, Sang-Min,Jang, Yeon-Sil,Lee, Choon-Taek,Kim, Young-Whan,Han, Sung-Koo,Shim, Young-Soo,Yoo, Chul-Gyu 대한결핵및호흡기학회 2010 Tuberculosis and Respiratory Diseases Vol.68 No.3
Background: Sepsis still has a high mortality rate despite adequate supportive care. Newer therapeutic modalities have been developed but they have generally ended in failure. Recently, insulin was reported to have an anti-inflammatory effect by inhibiting the $I{\kappa}B/NF-{\kappa}B$ pathway, and may have therapeutic potential in sepsis. However, the precise mechanism of the anti-inflammatory effect of insulin is unclear. This study examined the role of insulin in activating $I{\kappa}B/NF-{\kappa}B$ in macrophage. Methods: Raw 264.7 cells, a murine macrophage cell line, were used in this experiment. Western blotting using $I{\kappa}B$ Ab and phosphor-specific $I{\kappa}B$ Ab was performed to evaluate the degradation and phosphorylation of $I{\kappa}B$ cells. For the $I{\kappa}B$ Kinase (IKK) activity, an immune complex kinase assay was performed. The level of interleukin-6 (IL-6) was measured by ELISA to determine the level of proinflammatory cytokine. Results: $I{\kappa}B{\alpha}$ degradation began 30 min after lipopolysaccharide (LPS) treatment. However, an insulin pretreatment suppressed the $I{\kappa}B{\alpha}$ degradation caused by the LPS treatment. The phosphorylation of $I{\kappa}B{\alpha}$ and IKK activity was also inhibited by the insulin pretreatment. Finally, the insulin pretreatment showed a tendency to suppress the induction of IL-6 by LPS. Conclusion: Insulin might have an anti-inflammatory effect though partial inhibition of the $I{\kappa}B/NF{\kappa}B$ pathway in macrophage cell lines.
재조합 BMP-7 유전자가 전달된 HEK 293 세포에 의한 누드 마우스에서의 뼈형성
정수연,장원태,장연실,안면환,김재룡,송인환 영남대학교 의과대학 2003 Yeungnam University Journal of Medicine Vol.20 No.2
To induce bone formation at ectopic site by tissue engineering and gene therapy, we transplanted collagen sponges containing rhBMP-7 transduced HEK 293 cells in the hypodermis of nude mice. Bone formation was investigated by histological and electron microscopic method at 3, 6, and 9 weeks after transplantation. At 9 weeks after transplantation, eosinophilic bony tissue was observed in the implanted collagen sponge and was confirmed as bone tissue by Von Kossa stain. In the transmission electron microscopic observation, the cells in newly formed bone tissue had eccentrically located nucleus and well developed rough endoplasmic reticulum (rER). Therefore, the cells were evaluated as osteoblasts. Those results suggest that it is possible to form a bone tissue in the ectopic site by transplantation of rhBMP-7 transduced HEK 293 cells. This will be contributed to push more advanced gene therapy for bone formation. However, the HEK 293 cell is unable to apply to the clinical gene therapy. Therefore it is worth to find more compatible cells for clinical application. In addition, collagen sponge is considered as an excellent scaffold and/or carrier for gene therapy and a good biomaterial for tissue engineering.
대식세포주에서 인슐린이 IκB/NF-κB 경로 활성화에 미치는 영향
이상민 ( Sang Min Lee ),장연실 ( Yeon Sil Jang ),이춘택 ( Choon Taek Lee ),김영환 ( Young Whan Kim ),한성구 ( Sung Koo Han ),심영수 ( Young Soo Shim ),유철규 ( Chul Gyu Yoo ) 대한결핵 및 호흡기학회 2010 Tuberculosis and Respiratory Diseases Vol.68 No.3
Background: Sepsis still has a high mortality rate despite adequate supportive care. Newer therapeutic modalities have been developed but they have generally ended in failure. Recently, insulin was reported to have an anti-inflammatory effect by inhibiting the IκB/NF-κB pathway, and may have therapeutic potential in sepsis. However, the precise mechanism of the anti-inflammatory effect of insulin is unclear. This study examined the role of insulin in activating IκB/NF-κB in macrophage. Methods: Raw 264.7 cells, a murine macrophage cell line, were used in this experiment. Western blotting using IκB Ab and phosphor-specific IκB Ab was performed to evaluate the degradation and phosphorylation of IκB cells. For the IκB Kinase (IKK) activity, an immune complex kinase assay was performed. The level of interleukin-6 (IL-6) was measured by ELISA to determine the level of proinflammatory cytokine. Results: IκBα degradation began 30 min after lipopolysaccharide (LPS) treatment. However, an insulin pretreatment suppressed the IκBα degradation caused by the LPS treatment. The phosphorylation of IκBα and IKK activity was also inhibited by the insulin pretreatment. Finally, the insulin pretreatment showed a tendency to suppress the induction of IL-6 by LPS. Conclusion: Insulin might have an anti-inflammatory effect though partial inhibition of the IκB/NFκB pathway in macrophage cell lines.
박상언 ( Sang Un Park ),최은숙 ( Eun Sook Choi ),장연실 ( Yeon Sil Jang ),홍승희 ( Seung Hee Hong ),김인후 ( In Hoo Kim ),장동경 ( Dong Kyung Chang ) 대한소화기학회 2011 대한소화기학회지 Vol.57 No.3
Background/Aims: Tetraploid cells are frequently observed in the inflamed mucosal epithelial cells of the patients with Barrett`s esophagus or chronic ulcerative colitis. Polyploidy often occurs during cell fusion, abortive cell cycle, and endoreplication. Most tetraploid cells are engaged to apoptotic pathway, but some remaining stable tetraploid cells consequently cause aneuploidization and chromosomal instability. We investigated whether tetraploid cells could acquire survival advantage and hold a dominant position for natural selection. Methods: We established tetraploid cell line (HCT116GH) from parental diploid colorectal cancer cell line (HCT116) via PEG-mediated cell fusion and compared its cell viability, cell cycle response and apoptotic fractions responded to H2O2 with diploid HCT116 and p53 suppressed HCT116/H6 cell lines. Results: Using MTT assay, plating efficiency and clonogenicity, we evaluated the survival of each cell line. Tetraploid cell line HCT116GH demonstrated an 83 fold greater resistance to 100 μM H2O2 than the parental diploid HCT116, and 6 fold greater than even the p53 negative diploid HCT116/E6. Cellular sensitivity, G2/M arrests, and apoptotic proportion were observed less in response to H2O2 in HCT116GH compared with HCT116 and HCT116/E6. HCT116GH expressed lower level of p53 and p21 than diploid HCT116. Conclusions: Stable tetraploid cell lines showed enhanced viability in comparison to parental diploid cell lines. The enhanced viability observed in tetraploidization surpassed that from downregulation of p53. Frequent appearance of tetraploid cells in stressful condition can be caused by natural selection owing to their enhanced viability and may consequently contribute to cancer cell transformation.(Korean J Gastroenterol 2011;57:150-157)