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마이크로스트립-슬롯트 선로에 의한 광대역 마이크로파 Balun
윤영철,장익수,박기수,Yun, Yeong-Cheol,Jang, Ik-Su,Park, Gi-Su 대한전자공학회 1981 전자공학회지 Vol.18 No.6
마이크로스트립선로에 슬롯트선로를 결합시켜 평면형 광변역 balun을 설계, 제작하였다. 특히 C-band(4-8 GHz)에서 완전하게 동작시키기 위하여 슬롯트선로의 특성임피던스를 보상하여 주었으며, 이로써 이론치와 일치되는 결과를 얻을 수 있었다. 즉. 2 : 1의 부하저항에 대하여 Chebyshev 3-section 변환기로 정합회로를 구성한 결과. 3.5GHz∼7.0GHz의 1 -octave 대역에서 1.2 : 1 이하의 V.S.W.R.을 얻었으며 전송손실은 0.9dB까지 측정되었다. 특히 평형출력의 위상차는 180°±5°이내에서 linear 하게 변화하는 특성을 보이고 있다. By using a slot-line in combination with microstrip lines, a coplanar wide-band balun is designed and fabricated. The slot-line of balun junction is compensated to be operated in C-band(4~8GHz), and therefore the results are agreement with theoritical prediction. Experimental data are given for a 3-section Chebyshev transformer-matched balun with a balanced-to-unbalanced line impedance ratio of 2 : 1. A bandwidth from 3.5GHz to 7.0GHz is obtained with V.S.W.R. of below 1.2 : 1. Maximum insertion loss is measured as 0.9dB, and the phase difference varies linearlly within 180$^{\circ}$$\pm$5$^{\circ}$.
쥐 해마 절편배양에서 베타-아밀로이드 1-42분획 독성에 대한 (-)-Epigallocatechin Gallate의 효과
윤영철 대한신경과학회 2005 대한신경과학회지 Vol.23 No.6
Background: Considerable evidences suggest that the β-amyloid acts as a neurotoxin, and the epigallocatechin-3- gallate (EGCG) has the anti-inflammatory and anti-oxidant properties. The purpose of this study was to investigate whether the EGCG reduces the death of the cultured hippocampal tissues exposed to the β-amyloid 1-42 fragments (Aβ1-42). Method: We cultured the hippocampus of postnatal 7 days old Sprague-Dawley rat into slices of 450 µm. The tissue slices had been exposed with 100 µM Aβ1-42 at an interval of 3 days since 12 DIV (days in vitro). Following co-treatment of the tissue with 10 µM EGCG and Aβ1-42, we evaluated EGCG effect on Aβ1-42 induced neurotoxicity by measuring the expression of Bcl-2 and NeuN protein and by morphological observation of the hippocampus slice cultures with propidium iodide (PI) and bromodeoxyuridine (BrdU) staining. Results: The EGCG exerted a significant role in restoration of NeuN protein expression inhibited by Aβ1-42, showed inhibitory effects fluorescence in PI stained tissues, and increased the anti-BrdU stained cell. Conclusions: 10 µM EGCG reduced the Aβ1-42 induced neurotoxicity of the hippocampus slice culture.
윤영철,Ging-Yuek Robin Hsiung 대한치매학회 2015 Dementia and Neurocognitive Disorders Vol.14 No.4
Background and Purpose One of the most common genetic causes of frontotemporal dementia (FTD) is mutation in the progranulin(PGRN) gene. The aim of this study is to assess the early effects of the PGRN mutations on brain volumes by longitudinal voxel based morphometric(VBM) evaluation in asymptomatic mutation carriers. Methods We recruited 17 asymptomatic members of families with FTD caused by PGRN mutations; 7 mutation carriers (51.0±11.6 yr)and 10 non-carriers (55.2±6.0 yr, p=0.404). The MRI follow-up intervals of carriers and non-carriers were 788.6±103.8 and 922.0±225.1 days(p=0.124) respectively. We performed cross-sectional and longitudinal VBM analysis on both groups. Results At baseline, the carriers had lower white matter (WM) volumes in left frontal regions (p<0.001, uncorrected), but had no gray matter(GM) volume reduction. The carrier’s global GM (p=0.924) and WM volume (p=0.364) reduction rate were not different from the noncarrier’s. However, statistical parametric mapping T-maps showed differentially increased GM volume reductions in the bilateral parietal areasof carriers (p<0.001, uncorrected). Conclusions The findings from this study to examine WM and GM cross-sectional and longitudinal changes in PGRN mutation carrierssuggest that WM atrophic changes could precede both GM changes and symptom onset in FTD. Asymptomatic PGRN mutation carriershave measurably higher rates of regional GM atrophy than non-carriers even in the pre-dementia stages.