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수리동력학적 분리장치에 의한 고속 도로 강우유출수의 전처리 기술
우강화(Yu, Jianghua),이치타오(Yi, Qitao),김필주(Kim, Phil-Ju),여미미(Lu, Wei Wei),박성순(Park, Sung-Soon),김영철(Kim, Y.C.) 한국산학기술학회 2009 한국산학기술학회 학술대회 Vol.- No.-
고속도로 교량이나 성토지역 노면이 제공하는 자연적인 위치에너지(동력)를 활용하여 수리학적인 입자상 오염물질 분리장치를 실험실 조건에서 운전한 결과 운전압력 0.5기압(수두 5.6m) 이상에서 90% 이상의 제거효율을 보였다. D50는 약45μm이었는데 입자의 크기가 45 μm 보다 굵은 입자는 거의 대부분제거되지만 45 μm보다 작은 입자의 제거는 쉽지 않음을 시사해주고 있다. 이러한 입자를 제거하기 위한 후속장치가 필요하며 장치의 원활한 운전을 위해서 유지관리문제에 대한 치밀한 검토가 필요하다.
Zhongwei Zhang,Caiping Song,Tao Wang,Lei Sun,Ling Qin,Jianghua Ju 대한약학회 2021 Archives of Pharmacal Research Vol.44 No.2
Pathological retinal neovascularization is adriver of the progression of diabetic retinopathy (DR). Thepresent study sought to identify the microRNAs (miRNAs)that are diff erentially expressed during the progression ofDR as well as to explore the specifi c regulatory mechanismof those miRNAs in retinal neovascularization. Using amicroarray data set and a diabetic mouse model, it was determinedthat miR-139-5p was signifi cantly upregulated duringthe progression of DR. The in vitro investigation revealedan elevation in the miR-139-5p level in both the high glucose(HG)-treated mouse retinal microvascular endothelialcells (mRMECs) and the HG-treated human RMECs(hRMECs). The miR-139-5p overexpression elevated cellmigration, facilitated tube formation, and increased vascularendothelial growth factor (VEGF) protein level in thehRMECs. While the angiogenic eff ect of miR-139-5p overexpressionwas halted by an anti-VEGF antibody. Meanwhile,the miR-139-5p knockdown eliminated the VEGFinducedcell migration and tube formation in the hRMECs. The phosphatase and tensin homolog (PTEN) was the targetgene of the miR-139-5p. PTEN overexpression removed theangiogenic eff ect of miR-139-5p overexpression, which ledto reduced cell migration and tube formation. In the diabeticmice, the miR-139-5p antagomir eff ectively decreased theacellular capillaries and suppressed the formation of aberrantblood vessels in the retinal tissues. Taken together, miR-139-5p promotes retinal neovascularization by repressingPTEN expression.