http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Shou‑Dong Chai,Zhen‑Kun Li,Rui Liu,Tao Liu,Ming‑Feng Dong,Pei‑Zhe Tang,Jian‑Tang Wang,Sheng‑Jun Ma 대한독성 유전단백체 학회 2020 Molecular & cellular toxicology Vol.16 No.3
Background Nisoldipine can effectively suppress pulmonary arterial smooth muscle cell proliferation and c-Fos expression. Objective To identify the mechanism of the anti-inflammatory effects in monocrotaline-induced pulmonary arterial hypertension (PAH), focusing on the c-Fos/NLRP3/caspase-1 pathway. Results In a mice model of monocrotaline-induced PAH, miRNA-155 expression was increased. In an in vitro model, overexpression of miRNA-155 promoted inflammation and induced c-Fos, NLRP3, and caspase-1 protein expression. The inhibition of c-Fos reduced the effects of miRNA-155 on inflammation in an in vitro model of monocrotaline-induced PAH. The inhibition of NLRP3 reduced the effects of miRNA-155 on inflammation in an in vitro model of monocrotaline-induced PAH. Conclusions miRNA-155 increased inflammation in monocrotaline-induced PAH through c-Fos/NLRP3/caspase-1.
ADAPTIVE SLIDING MODE CONTROL OF LATERAL STABILITY OF FOUR WHEEL HUB ELECTRIC VEHICLES
Shou-Tao Li,Hui Liu,Di Zhao,Qiu-Yuan Li,Yantao Tian,De-Jun Wang,Ding-Li Yu 한국자동차공학회 2020 International journal of automotive technology Vol.21 No.3
Some physical parameters of a hub motor-driven four-wheel electric vehicle will change when the vehicle turns or maneuvers and the parameter change is caused by the change of the driving conditions. An adaptive sliding mode control is proposed in this paper to maintain the vehicle’s stability by compensating for the change of these parameters. The control parameter being adapted is the converging rate of the system state towards the sliding mode. As the Lyapunov method is used, so both the vehicle stability and adaptive rate convergence are guaranteed. Moreover, the hierarchical control structure is adopted for this vehicle stability control system. The above adaptive sliding model control forms the upper-layer; while the lower-layer control is to distribute the upper torque to the four wheels in an optimal way, subject to several constraints. In addition, the best feasible reference of the yaw rate and the vehicle side slip angle are obtained and used in the control system. The developed method is simulated under the CarSim/MATLAB co-simulation environment to evaluate the system performance. The simulation results are compared with the non-adaptive existing sliding mode control, and show that the proposed method is superior under different conditions.
Mechanistic Analysis of Taxol-induced Multidrug Resistance in an Ovarian Cancer Cell Line
Wang, Ning-Ning,Zhao, Li-Jun,Wu, Li-Nan,He, Ming-Feng,Qu, Jun-Wei,Zhao, Yi-Bing,Zhao, Wan-Zhou,Li, Jie-Shou,Wang, Jin-Hua Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.9
Objectives: To establish a taxol-resistant cell line of human ovarian carcinoma (A2780/Taxol) and investigate its biological features. Methods: The drug-resistant cell line (A2780/Taxol) was established by continuous stepwise selection with increasing concentrations of Taxol. Cell morphology was assessed by microscopy and growth curves were generated with in vitro and in vivo tumor xenograft models. With rhodamine123 (Rh123) assays, cell cycle distribution and the apoptotic rate were analyzed by flow cytometry (FCM). Drug resistance-related and signal associated proteins, including P-gp, MRPs, caveolin-1, PKC-${\alpha}$, Akt, ERK1/2, were detected by Western blotting. Results: A2780/Taxol cells were established with stable resistance to taxol. The drug resistance index (RI) was 430.7. Cross-resistance to other drugs was also shown, but there was no significant change to radioresistance. Compared with parental cells, A2780/Taxol cells were significantly heteromorphous, with a significant delay in population doubling time and reduced uptake of Rh123 (p<0.01). In vivo, tumor take by A2780 cells was 80%, and tumor volume increased gradually. In contrast, with A2780/Taxol cells in xenograft models there was no tumor development. FCM analysis revealed that A2780/Taxol cells had a higher percentage of G0/G1 and lower S phase, but no changes of G2 phase and the apoptosis rate. Expression of P-gp, MRP1, MRP2, BCRP, LRP, caveolin-1, PKC-${\alpha}$, Phospho-ERK1/2 and Phospho-JNK protein was significantly up-regulated, while Akt and p38 MARK protein expression was not changed in A2780/Taxol cells. Conclusion: The A2780/Taxol cell line is an ideal model to investigate the mechanism of muti-drug resistance related to overexpression of drug-resistance associated proteins and activation of the PKC-${\alpha}/ERK$ (JNK) signaling pathway.
Li-Jun Jia,Shou-Fa Zhang,Nian-Chao Qian,Xue-Nan Xuan,Long-Zheng Yu,Xue-Mei Zhang,Ming-Ming Liu 대한기생충학열대의학회 2013 The Korean Journal of Parasitology Vol.51 No.2
Neospora caninum is the etiologic agent of bovine neosporosis, which affects the reproductive performance of cattle worldwide. The transmembrane protein, NcSRS2, and dense-granule protein, NcGRA7, were identified as protective antigens based on their ability to induce significant protective immune responses in murine neosporosis models. In the current study, NcSRS2 and NcGRA7 genes were spliced by overlap-extension PCR in a recombinant adenovirus termed Ad5-NcSRS2-NcGRA 7, expressing the NcSRS2-NcGRA7 gene, and the efficacy was evaluated in mice. The results showed that the titer of the recombinant adenovirus was 109TCID50/ml. Three weeks post-boost immunization (w.p.b.i.), the IgG antibody titer in sera was as high as 1:4,096. IFN-γ and IL-4 levels were significantly different from the control group (P<0.01). This research established a solid foundation for the development of a recombinant adenovirus vaccine against bovine N. caninum.
Human Liver Specific Transcriptional Factor TCP10L Binds to MAD4
( Dao Jun Jiang ),( Hong Xiu Yu ),( Sa Yin Hexige ),( Ze Kun Guo ),( Xiang Wang ),( Li Jie Ma ),( Zheng Chen ),( Shou Yuan Zhao ),( Long Yu ) 생화학분자생물학회 2004 BMB Reports Vol.37 No.4
A human gene T-complex protein 10 like (TCP10L) was cloned in our lab. A previous study showed that it expressed specifically in the liver and testis. A transcription experiment revealed that TCP10L was a transcription factor with transcription inhibition activity. In this study, the human MAD4 was identified to interact with TCP10L by a yeast two-hybrid screen. This finding was confirmed by immunoprecipitation and subcellular localization experiments. As MAD4 is a member of the MAD family, which antagonizes the functions of MYC and promotes cell differentiation, the biological function of the interaction between TCP10L and MAD4 may be to maintain the differentiation state in liver cells. Also, we propose that the up-regulation of Myc is caused by the down-regulation of TCPIOL in human hepatocarcinomas.
Human Liver Specific Transcriptional Factor TCP10L Binds to MAD4
Jiang, Dao-Jun,Yu, Hong-Xiu,Hexige, Sa-Yin,Guo, Ze-Kun,Wang, Xiang,Ma, Li-Jie,Chen, Zheng,Zhao, Shou-Yuan,Yu, Long Korean Society for Biochemistry and Molecular Biol 2004 Journal of biochemistry and molecular biology Vol.37 No.4
A human gene T-complex protein 10 like (TCP10L) was cloned in our lab. A previous study showed that it expressed specifically in the liver and testis. A transcription experiment revealed that TCP10L was a transcription factor with transcription inhibition activity. In this study, the human MAD4 was identified to interact with TCP10L by a yeast two-hybrid screen. This finding was confirmed by immunoprecipitation and subcellular localization experiments. As MAD4 is a member of the MAD family, which antagonizes the functions of MYC and promotes cell differentiation, the biological function of the interaction between TCP10L and MAD4 may be to maintain the differentiation state in liver cells. Also, we propose that the up-regulation of Myc is caused by the down-regulation of TCP10L in human hepatocarcinomas.
Serum Macrophage Migration Inhibitory Factor as a Biomarker of Active Pulmonary Tuberculosis
Zhong-bo Shang,Jun Wang,Shou-gang Kuai,Yin-yin Zhang,Qin-fang Ou,Hao Pei,Li Hua Huang 대한진단검사의학회 2018 Annals of Laboratory Medicine Vol.38 No.1
Background: Macrophage migration inhibitory factor (MIF), a pro-inflammatory cytokine with chemokine-like functions, has been shown to play a central role in several acute and chronic inflammatory diseases. However, limited information is available regarding the use of MIF as an inflammatory pathway marker in patients with tuberculosis. This study aimed to investigate the association of MIF with IFN-γ and TNF-α in active pulmonary tuberculosis (APTB) following anti-tuberculosis treatment. Methods: The MIF, TNF-α, and IFN-γ serum levels were determined in 47 patients with APTB by cytokine-specific ELISA at four phases: prior to anti-tuberculosis drug treatment (baseline), and following 2, 4, and 6 months of treatment. In addition, we measured the MIF, TNF-α, and IFN-γ serum levels in 50 health controls. Results: MIF serum levels were significantly elevated (P<0.05) in patients with APTB prior to treatment compared with that in control subjects, and TNF-α ≥449.7 pg/mL was associated with high MIF levels (≥13.1 ng/mL). MIF levels were significantly reduced (P<0.01) following 2, 4, and 6 months of treatment, with variations in TNF-α and IFN-γ serum levels. MIF levels were positively correlated with the paired TNF-α level at baseline (r=0.1103, P=0.0316) and following 6 months of treatment (r=0.09569, P=0.0364).Conclusions: A reduction in the MIF serum levels in patients with APTB following anti-tuberculosis treatment may positively affect host immune protection against Mycobacterium tuberculosis infection. Thus, serum MIF levels may constitute a useful marker for assessing therapy effectiveness in patients with APTB.
Song, Qing-Kun,Li, Jing,Huang, Rong,Fan, Jin-Hu,Zheng, Rong-Shou,Zhang, Bao-Ning,Zhang, Bin,Tang, Zhong-Hua,Xie, Xiao-Ming,Yang, Hong-Jian,He, Jian-Jun,Li, Hui,Li, Jia-Yuan,Qiao, You-Lin,Chen, Wan-Qin Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.22
Background: The study aimed to describe the age distribution of breast cancer diagnosis among Chinese females for comparison with the United States and the European Union, and provide evidence for the screening target population in China. Materials and Methods: Median age was estimated from hospital databases from 7 tertiary hospitals in China. Population-based data in China, United States and European Union was extracted from the National Central Cancer Registry, SEER program and GLOBOCAN 2008, respectively. Age-standardized distribution of breast cancer at diagnosis in the 3 areas was estimated based on the World Standard Population 2000. Results: The median age of breast cancer at diagnosis was around 50 in China, nearly 10 years earlier than United States and European Union. The diagnosis age in China did not vary between subgroups of calendar year, region and pathological characteristics. With adjustment for population structure, median age of breast cancer at diagnosis was 50~54 in China, but 55~59 in United States and European Union. Conclusions: The median diagnosis age of female breast cancer is much earlier in China than in the United States and the European Union pointing to racial differences in genetics and lifestyle. Screening programs should start at an earlier age for Chinese women and age disparities between Chinese and Western women warrant further studies.