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Yun Deng,Yali Luo,Bingjun Qian,Zhenmin Liu,Yuanrong Zheng,Xiaoyong Song,Shaojuan Lai,Yanyun Zhao 한국식품과학회 2014 Food Science and Biotechnology Vol.23 No.2
The antihypertensive activity of few-flower wildrice was studied in spontaneously hypertensive rats (SHRs)with evaluation of blood pressure lowering effects andtranscriptional levels of the sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) gene that is regulated by AngiotensinII (Ang II). SHRs were randomly divided into 5 groupswith 6 rats each. The systolic blood pressure (SBP) reachedthe lowest point 3 h after administration of a single dose ofpaste made from few-flower wild rice stem powder. TheSBP of SHR in the relatively high amount of RSP (HRSP)administrated group was reduced by approximately 30mmHg, compared to the negative control group, and wasnot significantly different from the positive control IPPcontrol group at a dose of 1.5 mg/kg body weight (p>0.05). RSP administrated SHRs showed a significantly higherSERCA2a transcription level than negative control SHRs(p<0.05). RSP administration had no negative effects onglycometabolism of SHR.
( Yun Deng ),( Yong Qing Li ),( Xiong Wei Fan ),( Wu Zhou Yuan ),( Hua Ping Xie ),( Xiao Yang Mo ),( Yan Yan ),( Jun Mei Zhou ),( Yue Qun Wang ),( Xian Li Ye ),( Yong Qi Wan ),( Xiu Shan Wu ) 생화학분자생물학회 (구 한국생화학분자생물학회) 2010 BMB Reports Vol.43 No.6
LBH is a transcription factor as a candidate gene for CHD associated with partial trisomy 2p syndrome. To identify potential LBH-interacting partners, a yeast two-hybrid screen using LBH as a bait was performed with a human heart cDNA library. One of the clones identified encodes αB-crystallin. Co-immunoprecipitation and GST pull-down assays showed that LBH interacts with αB-crystallin, which is further confirmed by mammalian two-hybrid assays. Co-localization analysis showed that in COS-7 cells, αB-crystallin that is cytoplasmic alone, accumulates partialy in the nucleus when co-transfected with LBH. Transient transfection assays indicated that overexpression of LBH or αB-crystallin reduced the transcriptional activities of p53 and p21, respectively, Overexpression of both αB-crystallin and LBH together resulted in a stronger repression of the transcriptional activities of p21 and p53. These results showed that the interaction of LBH and αB-crystallin may inhibit synergistically the transcriptional regulation of p53 and p21. [BMB reports 2010; 43(6): 432-437]
Deng, Yun,Zhao, Jian,Sakurai, Daisuke,Sestak, Andrea L,Osadchiy, Vadim,Langefeld, Carl D,Kaufman, Kenneth M,Kelly, Jennifer A,James, Judith A,Petri, Michelle A,Bae, Sang-Cheol,Alarcó,n-Riquelme, H. K. Lewis 2016 Annals of the rheumatic diseases Vol.75 No.11
<B>Objectives</B><P>Following up the systemic lupus erythematosus (SLE) genome-wide association studies (GWAS) identification of <I>NMNAT2</I> at rs2022013, we fine-mapped its 150 kb flanking regions containing <I>NMNAT2</I> and <I>SMG7</I> in a 15 292 case-control multi-ancestry population and tested functions of identified variants.</P><B>Methods</B><P>We performed genotyping using custom array, imputation by IMPUTE 2.1.2 and allele specific functions using quantitative real-time PCR and luciferase reporter transfections. SLE peripheral blood mononuclear cells (PBMCs) were cultured with small interfering RNAs to measure antinuclear antibody (ANA) and cyto/chemokine levels in supernatants using ELISA.</P><B>Results</B><P>We confirmed association at <I>NMNAT2</I> in European American (EA) and Amerindian/Hispanic ancestries, and identified independent signal at <I>SMG7</I> tagged by rs2702178 in EA only (p=2.4×10<SUP>−8</SUP>, OR=1.23 (95% CI 1.14 to 1.32)). In complete linkage disequilibrium with rs2702178, rs2275675 in the promoter region robustly associated with <I>SMG7</I> mRNA levels in multiple expression quantitative trait locus (eQTL) datasets. Its risk allele was dose-dependently associated with decreased <I>SMG7</I> mRNA levels in PBMCs of 86 patients with SLE and 119 controls (p=1.1×10<SUP>−3</SUP> and 6.8×10<SUP>−8</SUP>, respectively) and conferred reduced transcription activity in transfected HEK-293 (human embryonic kidney cell line) and Raji cells (p=0.0035 and 0.0037, respectively). As a critical component in the nonsense-mediated mRNA decay pathway, SMG7 could regulate autoantigens including ribonucleoprotein (RNP) and Smith (Sm). We showed <I>SMG7</I> mRNA levels in PBMCs correlated inversely with ANA titres of patients with SLE (r=−0.31, p=0.01), and <I>SMG7</I> knockdown increased levels of ANA IgG and chemokine (C-C motif) ligand 19 in SLE PBMCs (p=2.0×10<SUP>−5</SUP> and 2.0×10<SUP>−4</SUP>, respectively).</P><B>Conclusion</B><P>We confirmed <I>NMNAT2</I> and identified independent <I>SMG7</I> association with SLE. The inverse relationship between levels of the risk allele-associated <I>SMG7</I> mRNAs and ANA suggested the novel contribution of mRNA surveillance pathway to SLE pathogenesis.</P>
( Yun Deng ),( Bi Sheng Liu ),( Xiong Wei Fan ),( Yue Qun Wang ),( Ming Tang ),( Xiao Yang Mo ),( Yong Qing Li ),( Zao Chu Ying ),( Yong Qi Wan ),( Na Luo ),( Jun Mei Zhou ),( Xiu Shan Wu ),( Wu Zhou 한국생화학분자생물학회 (구 한국생화학회) 2010 BMB Reports Vol.43 No.3
In this study, we report the identification and characterization of a novel C2H2 zinc finger protein, ZNF552, from a human embryonic heart cDNA library. ZNF552 is composed of three exons and two introns and maps to chromosome 19q13.43. The cDNA of ZNF552 is 2.3 kb, encoding 407 amino acids with an amino-terminal KRAB domain and seven carboxyl-terminal C2H2 zinc finger motifs in the nucleus and cytoplasm. Northern blotting analysis indicated that a 2.3 kb transcript specific for ZNF552 was expressed in liver, lung, spleen, testis and kidney, especially with a higher level in the lung and testis in human adult tissues. Reporter gene assays showed that ZNF552 was a transcriptional repressor, and overexpression of ZNF552 in the COS-7 cells inhibited the transcriptional activities of AP-1 and SRE, which could be relieved through RNAi analysis. Deletion studies showed that the KRAB domain of ZNF552 may be involved in this inhibition. [BMB reports 2010; 43(3): 193-198]
Staged Improvement in Awareness of Disease for Elderly Cancer Patients in Southern China
Li, Xing,Dong, Min,Wen, Jing-Yun,Wei, Li,Ma, Xiao-Kun,Xing, Yan-Fang,Deng, Yun,Chen, Zhan-Hong,Chen, Jie,Ruan, Dan-Yun,Lin, Ze-Xiao,Wang, Tian-Tian,Wu, Dong-Hao,Liu, Xu,Hu, Hai-Tao,Lin, Jia-Yu,Li, Zhu Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.15
Background: In mainland China, awareness of disease of elderly cancer patients largely relies on the patients' families. We developed a staged procedure to improve their awareness of disease. Materials and Methods: Participants were 224 elderly cancer patients from 9 leading hospitals across Southern China. A questionnaire was given to the oncologists in charge of each patient to evaluate the interaction between family and patients, patient awareness of their disease and participation in medical decision-making. After first cycles of treatment, increased information of disease was given to patients with cooperation of the family. Then patient awareness of their disease and participation in medical decision-making was documented. Results: Among the 224 cancer elderly patients, 26 (11.6%) made decisions by themselves and 125 (55.8%) delegated their rights of decision-making to their family. Subordinate family members tended to play a passive role in decision-making significantly. Patients participating more in medical decision-making tended to know more about their disease. However, in contrast to the awareness of disease, patient awareness of violation of medical recommendations was reversely associated with their participation in medical decision-making. Improvement in awareness of diagnosis, stages and prognosis was achieved in about 20% elderly cancer patients. About 5% participated more actively in medical decision-making. Conclusions: Chinese elderly cancer patient awareness of disease and participation in medical decision-making is limited and relies on their family status. The staged procedure we developed to improve patient awareness of disease proved effective.
Meta-analysis of the CYP1A2 -163C>A Polymorphism and Lung Cancer Risk
Deng, Sheng-Qiong,Zeng, Xian-Tao,Wang, Yun,Ke, Qing,Xu, Qiong-Li Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.5
Many published studies have concerned associations between the CYP1A2 -163 C>A polymorphism and risk of lung cancer, but the results have been inconsistent. Therefore, we performed a meta-analysis to obtain a more precise estimate. We searched the PubMed database up to March 1, 2013 for relevant cohort and case-control studies. Supplementary search was conducted manually by searching the references of the included studies and relevant meta-analyses. A meta-analysis was performed using RevMan 5.2 software for calculation of pooled odds ratios (ORs) and relevant 95% confidence intervals (CIs) after data extraction. Finally, seven case-control studies and one nested case-control study involving 1,675 lung cancer patients and 2,393 controls were included. The meta-analysis showed that there was no association of CYP1A2 -163 C>A polymorphism with risk of lung cancer overall [(OR=0.89, 95%CI= 0.74-1.07) for C vs. A; (OR=0.73, 95%CI= 0.50-1.07) for AA vs. CC ; (OR=0.82, 95%CI= 0.62-1.09) for AC vs. CC; (OR=0.79, 95%CI= 0.58-1.07) for (AC+AA) vs. CC; and (OR=0.87, 95%CI= 0.67-1.13) for AA vs. (CC+AC)]. Subgroup analysis indicated that there was an associationbetween CYP1A2 -163C>A polymorphism and lung cancer risk for population-based controls, a trend risk for SCCL (squamous cell carcinoma of lung) and Caucasians. These results suggested that -163 C>A polymorphism is likely to be associated with risk of lung cancer compared with population-based controls.