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UWB MB-OFDM 시스템에서 TOA 성능향상을 위한 동기화 기법
권형주,이준호,정영석,조상호,Kwon, Hyung-Ju,Lee, Joon-Ho,Jeong, Yeong-Suk,Jo, Sang-Ho 한국통신학회 2007 韓國通信學會論文誌 Vol.32 No.5c
We propose how to improve the performance of TOA estimation in UWB MB-OFDM systems. The scheme is based on the correlation between the OFDM preamble and the template signal. The validity of the proposed scheme is shown using the simulation results, where it is shown that the performance of the proposed scheme outperforms that of the existing schemes IEEE 802.15.3a task group에서 채택한 4가지의 UWB 채널 모델과 AWGN 채널 모델에 대해서, MB-OFDEM 시스템의 preamble 신호를 이용한 TOA 성능 향상기법을 제안한다. 제안되는 방법은 수신 신호와 template 신호 사이의 correlation에 의한 타이밍 동기화 지점을 이용하여 TOA를 추정한다. 제안한 방법의 성능이 기존의 방법에 비하여 우수한 성능을 나타냄을 전산모의실험을 통하여 확인한다.
BRAF(V600E) 돌연변이 갑상선 역형성암에서 BRAF(V600E) 억제에 의한 EGFR 발현 증가가 표적치료에 대한 저항성발현과 상피-간질세포이행과정에 미치는 영향분석
변형권(Hyung Kwon Byeon),나휘정(Hwi Jung Na),양연주(Yeon Ju Yang),박재홍(Jae Hong Park),권형주(Hyeong Ju Kwon),장재원(Jae Won Chang),반명진(Myung Jin Ban),김원식(Won Shik Kim),신동엽(Dong Yeob Shin),이은직(Eun Jig Lee),고윤우(Yoon Wo 대한두경부종양학회 2014 대한두경부 종양학회지 Vol.30 No.2
Background and Objectives:Anaplastic thyroid carcinoma(ATC) is a rare but highly aggressive thyroid ma-lignancy that is associated with an extremely poor survival despite the best multidisciplinary care. BRAF(V600E) mutation is detected in about a quarter of ATC, but unlike its high treatment response to selective BRAF inhibitor (PLX4032) in metastatic melanoma, the treatment response of ATC is reported to be low. The purpose of this study is to investigate the innate resistance mechanism responsible for this low treatment response to BRAF inhibitor and its effect on epithelial-mesenchymal transition(EMT). Materials and Methods:Two ATP cell lines, 8505C and FRO were selected and treated with PLX4032 and its drug sensitivity and effects on cell migration and EMT were examined and compared. Further investigation on the changes in signals responsible for the different treatment response to PLX4032 was carried out and the same ex-periment was performed on both orthotopic and ectopic xenograft mouse models. Results:FRO cell line was more sensitive to PLX4032 treatment compared to 8505C cell line. The resistance to BRAF inhibition in 8505C was due to increased expression of EGFR. Effective inhibition of both EGFR and p-AKT was achieved after dual treatment with BRAF inhibitor(PLX4032) and EGFR inhibitor(Erlotinib). Similar results were confirmed on in vivo study. Conclusion:EGFR-mediated reactivation of the PI3K/AKT pathway and MAPK pathway contributes to the relative insensitivity of BRAF(V600E) mutant ATC cells to PLX4032. Dual inhibition of BRAF and EGFR leads to sustained treatment response including cell invasiveness.