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      • KCI등재

        Variation of sexual dimorphism and asymmetry in disease expression of inflammatory arthritis among laboratory mouse models with different genomic backgrounds

        Wei Dong,Cheng Tian,Z. Galvin Li,David Brand,Yanhong Cao,Xiaoyun Liu,Jiamin Ma,Andy Chai,LindaK.myers,Jian Yan,Karen Hasty,John Stuart,Yan Jiao,Weikuan Gu,Xiaojun Cai 한국실험동물학회 2023 Laboratory Animal Research Vol.39 No.4

        Sex difference has shown in the arthritis diseases in human population and animal models. We investigate how the sex and symmetry vary among mouse models with different genomic backgrounds. Disease data of sex and limbs accumulated in the past more than two decades from four unique populations of murine arthritis models were analyzed. They are (1) interleukin-1 receptor antagonist (IL-1ra) deficient mice under Balb/c background (Balb/c KO); (2) Mice with collagen II induced arthritis under DBA/1 background; (3) Mice with collagen II induced arthritis under C57BL/6 (B6) background and (4) A F2 generation population created by Balb/c KO X DBA/1 KO. Our data shows that there is a great variation in sexual dimorphism for arthritis incidence and severity of arthritis in mice harboring specific genetic modifications. For a F2 population, the incidence of arthritis was 57.1% in female mice and 75.6% in male mice. There was a difference in severity related to sex in two populations: B6.DR1/ B6.DR4 (P < 0.001) and F2 (P = 0.023) There was no difference Balb/c parental strain or in collagen-induced arthritis (CIA) in DBA/1 mice. Among these populations, the right hindlimbs are significantly higher than the scores for the left hindlimbs in males (P < 0.05). However, when examining disease expression using the collagen induced arthritis model with DBA/1 mice, sex-dimorphism did not reach statistical significance, while left hindlimbs showed a tendency toward greater disease expression over the right. Sexual dimorphism in disease expression in mouse models is strain and genomic background dependent. It sets an alarm that potential variation in sexual dimorphism among different racial and ethnic groups in human populations may exist. It is important to not only include both sexes and but also pay attention to possible variations caused by disease expression and response to treatment in all the studies of arthritis in animal models and human populations.

      • KCI등재

        ADAPTIVE AUTHORITY ALLOCATION OF HUMAN-AUTOMATION SHARED CONTROL FOR AUTONOMOUS VEHICLE

        Wu Yanhong,Wei Hanbing,Chen Xing,Xu Jin,Rahul Sharma 한국자동차공학회 2020 International journal of automotive technology Vol.21 No.3

        Great advances had been achieved in the discipline of environmental perception, motion planning and control strategy implementation, however, fully autonomous vehicle is still far from large-scale commercial application. The concept of “human-automation shared control” provides a promising solution to enhance autonomous driving safety, to which great research effort has been contributed in recent years. Nevertheless, more attention should be given to the following aspects. The present shared control strategy either only considers the discontinuous switching control between driver and ADS or investigates the simple effect of driver’s behavior in specific scenarios. The adaptive authority allocation between the driver’s active assistance and ADS hasn’t been investigated yet. In this paper, a shared control experiment with driver’s active assistance is conducted in scheduled traffic scenarios to observe the state of vehicle and arm’ EMG signal. After that, we construct a feature classification algorithm for shared control authority by clustering the experimental data. Then, a SCS with incremental PID controller and 2 DOF vehicle dynamic model is proposed. For validation of the SCS, the comparison of vehicle performance for different control authority illustrates that SCS can allocate appropriate control authority to improve the safety.

      • KCI등재

        PSCArs2294008 T polymorphism increases the risk of bladder cancer in Bai, Dai, and Han ethnicity in China and a potential mechanism

        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.

      • KCI등재

        MiR-182-5p Mediated by Exosomes Derived From Bone Marrow Mesenchymal Stem Cell Attenuates Inflammatory Responses by Targeting TLR4 in a Mouse Model of Myocardial Infraction

        Sun Chuang,Li Wei,Li Yanhong,Chen Jian,An Huixian,Zeng Guangwei,Wang Tingting,Guo Yazhou,Wang Changying 대한면역학회 2022 Immune Network Vol.22 No.6

        Exosomes derived from mesenchymal stem cells (MSCs) could protect against myocardial infarction (MI). TLR4 is reported to play an important role in MI, while microRNA-182-5p (miR-182-5p) negatively regulates TLR4 expression. Therefore, we hypothesize that MSCs-derived exosomes overexpressing miR-182-5p may have beneficial effects on MI. We generated bone marrow mesenchymal stem cells (BM-MSCs) and overexpressed miR-182-5p in these cells for exosome isolation. H2O2-stimulated neonatal mouse ventricle myocytes (NMVMs) and MI mouse model were employed, which were subjected to exosome treatment. The expression of inflammatory factors, heart function, and TLR4 signaling pathway activation were monitored. It was found that miR-182-5p decreased TLR4 expression in BM-MSCs and NMVMs. Administration of exosomes overexpressing miR-182-5p to H2O2-stimulated NMVMs enhanced cell viability and suppressed the expression of inflammatory cytokines. In addition, they promoted heart function, suppressed inflammatory responses, and de-activated TLR4/NF-κB signaling pathway in MI mice. In conclusion, miR-182-5p transferred by the exosomes derived from BM-MSCs protected against MI-induced impairments by targeting TLR4.

      • KCI등재

        Numerical simulation of resistance welding of solar cell using a thermal-electrical-mechanical coupled model

        Xiaohong Zhan,Qi Zhang,Zhenxin Zhu,Yanhong Wei 대한기계학회 2018 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.32 No.1

        A thermal-electrical-mechanical coupled model was established to simulate the Parallel-gap resistance welding (PGRW) process between the Germanium-based solar cell and the silver interconnector. The simulated results showed that the peak temperature during PGRW is lower than the melting temperature of the base material. It is indicated that the connection mechanism of PGRW was mainly the interdiffusion and recrystallization due to pressure of electrode and the resistance heat. A detailed calculation method of current was proposed using semi-layered resistance model and layered resistance model. By comparing these models, it was found that the layered resistance model was more accurate to calculate the current value. The maximum residual stress was generated within the region under the welding electrode, while the maximum deformation was generated on the edge of the interconnector. The current variation trend predicated by the simulation results is in good agreement with the results obtained by the experiments.

      • KCI등재

        Stability analysis of an axially moving free-free beam

        Han Guangcai,Liu Fei,Wu Yanhong,Wang Wei 대한기계학회 2020 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.34 No.5

        This study investigates the stability of an axially moving free-free beam as afunction of moving speed, modulus of elasticity, and axial tensile force. The mode shapes of thebeam under different axial tensile forces are also discussed. In this study, we derive the equationsof motion of a flexible free-free beam with a uniformly circular cross section that movesaxially at a constant speed. Using Galerkin’s technique, we dicretize and reduce the nonlinearpartial differential equation of motion to a set of ordinary differential equations by choosing theshape functions to be the eigenfunctions of a free beam. The state-space method is used toinvestigate the stability of an axially moving free beam for different cases. Numerically, the stabilityof the system is influenced by different cases in various ways and degrees. The transversevibration modes with different tensile forces are also considered in this study.

      • KCI등재

        TCP10L synergizes with MAD1 in transcriptional suppression and cell cycle arrest through mutual interaction

        ( 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]

      • KCI등재

        Transcriptomic analysis of cells in response to EV71 infection and 2Apro as a trigger for apoptosis via TXNIP gene

        Chenguang Yao,Kanghong Hu,Caili Xi,Ni Li,Yanhong Wei 한국유전학회 2019 Genes & Genomics Vol.41 No.3

        Background Enterovirus 71 (EV71) is the main pathogen of hand-foot-mouth disease (HFMD) and sometimes causes several neurological complications. However, the underlying mechanism of the host response to the virus infection remains unclear. Objective To reveal the cell-specific transcriptional response of cultured RD cells following infection with EV71, and better understand the molecular mechanisms of virus-host interactions. Methods The RD cells were infected with or without EV71 for 24 h, and then transcriptome sequencing and qRT-PCR were performed to analyze the transcriptome difference of functional genes. Results More than 15000 genes were identified in transcriptome sequencing. In comparison with uninfected RD cells, 329 DEGs were identified in cells infected with EV71. GO and KEGG pathway enrichment analysis showed that most of the DEGs were related to DNA binding, transcriptional regulation, immune response and inflammatory response, apoptosis inducing factors and enriched in JAK-STAT and MAPK signaling pathways. TXNIP (thioredoxin-interacting protein) gene was further demonstrated to play an important role participating in cellular apoptosis induced by EV71, and the apoptosis and death mediated by TXNIP during EV71 infection was triggered by viral 2A protease (2Apro), not 3C protease (3Cpro). Conclusion Our study demonstrated that RD cells have a significant response to EV71 infection, including immune response and apoptosis. 2Apro might be a key inducer relative to the cellular apoptosis and death mediated by TXNIP during EV71 infection. These data would contribute to preferably understand the process at the molecular level and provide theoretical foundation for diagnosis and treatment of EV71-related diseases.

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