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- 저자 : Yanhong Yu (검색결과 3 건)
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Yili Zhu,Yanhong Zhang,Chengtao Yu 대한기계학회 2020 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.34 No.6
A new-type active touchdown bearing (TDB) system integrated with a centering device to eliminate the protective clearance after rotor drop in an active magnetic bearing (AMB) system is proposed. A rotor dynamic model is established on the basis of rigid rotor theory. A collision model between the support base and outer race of the ball bearing and a real-time ball bearing elastic supporting force model are established on the basis of Hertz contact theory. The dynamic model of the new-type TDB is established on the basis of vibration theory. Using these established theoretical models, the dynamic responses after rotor drops onto the new-type TDB are simulated and compared with the responses after rotor drops onto traditional TDB. Relevant experiments are conducted on an AMB test platform to verify the simulation results. The results show that the proposed new-type TDB can rapidly eliminate the protective clearance after rotor drop and can thus effectively reduce the following rotor vibrations and impacts.
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( Suqin Shen ),( Jie Zuo ),( Huan Feng ),( Meirong Bai ),( Chenji Wang ),( Youheng Wei ),( Yanhong Li ),( Yichen Le ),( Jiaxue Wu ),( Yanhua Wu ),( Long Yu ) 생화학분자생물학회(구 한국생화학분자생물학회) 2016 BMB Reports Vol.49 No.6
T-complex protein 10A homolog 2 (TCP10L) was previously demonstrated to be a potential tumor suppressor in human hepatocellular carcinoma (HCC). However, little is known about the molecular mechanism. MAX dimerization protein 1 (MAD1) is a key transcription suppressor that is involved in regulating cell cycle progression and Myc-mediated cell transformation. In this study, we identified MAD1 as a novel TCP10L-interacting protein. The interaction depends on the leucine zipper domain of both TCP10L and MAD1. TCP10L, but not the interaction-deficient TCP10L mutant, synergizes with MAD1 in transcriptional repression, cell cycle G1 arrest and cell growth suppression. Mechanistic exploration further revealed that TCP10L is able to stabilize intracellular MAD1 protein level. Consistently, the MAD1-interaction-deficient TCP10L mutant exerts no effect on stabilizing the MAD1 protein. Taken together, our results strongly indicate that TCP10L stabilizes MAD1 protein level through direct interaction, and they cooperatively regulate cell cycle progression. [BMB Reports 2016; 49(6): 325-330]
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Junfeng Yang,Wei Li,Zhuorui Zhang,Jie Shen,Ningnan Zhang,Min Yang,Maolin Yang,Yanhong Yu 한국유전학회 2018 Genes & Genomics Vol.40 No.5
The aim of this study is to make a comparative evaluation on association of PSCArs2294008 C/T polymorphism with the risk of bladder cancer in Bai, Dai, and Han people in China. A potential mechanism of the T allele risk was also investigated. T allele increased the occurring risk of bladder cancer in Han (OR 1.34; 95% CI 1.17–1.69), Dai, (OR 1.33; 95% CI 1.12–1.70), and Bai (OR 1.14; 95% CI 1.08–1.57) people. T genotype was also observed to associate with invasive bladder cancer in all the three populations (Bai, OR 1.15, 95% CI 1.07–1.87; Dai, OR 1.17, 95% CI 1.05–2.23; Han, OR 1.22, 95% CI 1.10–2.09). PSCA m-RNA levels in T genotype bladder cancer tissues were significantly lower than those in C genotype. An enhancement of PSCA m-RNA level by over-expressing C or T genotype in bladder cancer cells both decreased the cell proliferation and migration, but not affected cell cycle. The increased cell apoptasis due to the over-expression of the two variants was observed. Those change of cell proliferation, migration, and apoptasis was more remarkable in over-expressed C genotype cells than those in over-expressed T genotype. T genotype was genetically high risk to the occurrence of bladder cancer. The decreased PSCA m-RNA levels were involved in the progress of bladder cancer. T allele takes more responsibility for PSCA m-RNA down-regulation to promote cell proliferation and migration and hinder cell apoptasis, thus leading to a higher risk.
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