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김회진(Kim, Hoijin),이정준(Yi, Zheongzun),박종섭(Park, Jongsup),강준석(Kang, Junsuk) 한국방재학회 2020 한국방재학회논문집 Vol.20 No.6
노후건축물과 국내 지진 발생빈도 및 강도의 증가에 따른 인명・재산 피해의 증가가 예상되어, 노후건축물의 지진 취약성및 위험성 분석이 요구되고 있다. 이에 노후건축물 지진 실험을 진행하여 위험도 도출을 위한 지표를 도출하고자 한다. 조적조 구조물에 초기 균열을 발생시켜 노후도를 반영하고, 노후되지 않은 대조군과 비교하여 노후도가 건물에 미치는 영향을분석하였다. 그 결과, 실험체인 조적벽은 내진성능을 만족하였으나 노후도를 고려한 실험체에서 초기 균열을 따라 국부적파괴가 발생하였고, 추가적인 균열이 발생하여 안전성이 크게 감소하였다. 이를 통하여 조적조 건축물의 노후화로 인한균열이 건축물의 내진성능을 크게 훼손시키는 것을 보여준다. Due to the increase in the frequency and intensity of earthquakes and the number of old buildings and in Korea, there is an expected increase in the damage to life and property. Therefore, we intend to derive an indicator to evaluate the risk level by conducting a seismic test on old buildings. An initial crack was generated in the masonry structure to reflect the deterioration. The effect of the deterioration on the building was subsequently analyzed by comparing it with the uncracked control group. As a result, the masonry wall, which was the specimen, satisfied the seismic performance, but local failure occurred along the initial crack in the specimen considering the aging. The safety was significantly decreased due to the occurrence of additional cracks. This demonstrates that the cracks caused by the aging of the masonry building greatly damaged the seismic performance of the building.
Byung-Hee Chung,김수곤,김종대,이정준,Yi-Yong Baek,정두일,이한수,최종선,하권수,원무호,권영근,김영명 생화학분자생물학회 2012 Experimental and molecular medicine Vol.44 No.3
Nitric oxide (NO) produced by endothelial NO synthase (eNOS) plays an important role in vascular functions,including vasorelaxation. We here investigated the pharmacological effect of the natural product syringaresinol on vascular relaxation and eNOS-mediated NO production as well as its underlying biochemical mechanism in endothelial cells. Treatment of aortic rings from wild type, but not eNOS-/- mice, with syringaresinol induced endothelium-dependent relaxation,which was abolished by addition of the NOS inhibitor NG-monomethyl-L-arginine. Treatment of human endothelial cells and mouse aortic rings with syringaresinol increased NO production, which was correlated with eNOS phosphorylation via the activation of Akt and AMP kinase (AMPK) as well as elevation of intracellular Ca2+ levels. A phospholipase C (PLC) inhibitor blocked the increases in intracellular Ca2+ levels,AMPK-dependent eNOS phosphorylation, and NO production, but not Akt activation, in syringaresinol-treated endothelial cells. Syringaresinol-induced AMPK activation was inhibited by co-treatment with PLC inhibitor, Ca2+ chelator, calmodulin antagonist,and CaMKKβ siRNA. This compound also increased eNOS dimerization, which was inhibited by a PLC inhibitor and a Ca2+-chelator. The chemicals that inhibit eNOS phosphorylation and dimerization attenuated vasorelaxation and cGMP production. These results suggest that syringaresinol induces vasorelaxation by enhancing NO production in endothelial cells via two distinct mechanisms, phosphatidylinositol 3-kinase/Akt- and PLC/Ca2+/CaMKKβ-dependent eNOS phosphorylation and Ca2+-dependent eNOS dimerization.