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51.
Li Nan Shi Hangyu Hou Pengfei Gao Lu Shi Yongqiang Mi Weiyang Zhang Gang Wang Ning Dai Wei Wei Lin Jin Tianbo Shi Yongzhi Guo Shiwen 《Functional & integrative genomics》2022,22(1):27-33
Functional & Integrative Genomics - This study ascertained to explore the potential contribution of ARRDC3 polymorphisms in the risk and prognosis of glioma. One thousand sixty-one patients and... 相似文献
52.
Min Dai Yuhong Chen Xiaodong Mei 《Biochemical and biophysical research communications》2019,508(1):225-229
Pravastatin sodium on triggering receptor expressed on myeloid cell-1 (TREM-1)-mediated inflammation in human peripheral blood mononuclear cells (PBMCs) has been poorly investigated. In this study, we isolated PBMCs from the peripheral blood samples of patients with chronic obstructive pulmonary disease, treated the cells with pravastatin sodium, and determined a concentration at which more than 90% cells could survive. Then we treated cells with 10?ng/ml of lipopolysaccharide, added with 10, 50, 100?μM of pravastatin sodium combined with or without LR-12, a known TREM-1 inhibitor. The expression of TREM-1 was determined by quantitative RT-PCR. The levels of TREM-1, IL-6, and TNF-α in cell culture supernatant were measured with ELISA. Simultaneously, NF-κB signaling pathway-related protein p-p65 and p-IκBα were detected by Western blot assay. Results demonstrated that pravastatin sodium significantly mitigated lipopolysaccharide-stimulated TREM-1 over-expression at mRNA and protein levels dose-dependently. Elevated IL-6 and TNF-α levels changed synchronously. LR-12 inhibited the TREM-1 over-expression and inflammatory factor production but did not show extra synergistic effect to pravastatin. Lipopolysaccharide induced phospho-p65 and -IκBα over-expression was weakened significantly when cells were treated with pravastatin sodium. In conclusion, pravastatin could inhibit TREM-1-medieted inflammation and NF-κB signaling pathway was involved. 相似文献
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Bingchuan Wei Nicholas Woon Lu Dai Raphael Fish Michelle Tai Winode Handagama Ashley Yin Jia Sun Andrew Maier Dana McDaniel Elvira Kadaub Jessica Yang Miguel Saggu Ann Woys Oxana Pester Danny Lambert Alex Pell Zhiqi Hao Gordon Magill Jack Yim Jefferson Chan Lindsay Yang Frank Macchi Christian Bell Galahad Deperalta Yan Chen 《MABS-AUSTIN》2022,14(1)
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56.
Ruilong Zhang Zhiping Zhou Yi Wang Xiaohui Dai Li Chen Jiangdong Dai 《仿生工程学报(英文版)》2021,18(3):559-573
Mimicry of nature drives the development of bionic materials.Bionic superhydrophobic materials are a kind of high-efficiency materials to handle oil spills and ... 相似文献
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58.
Miao L Dai Y Zhang J 《American journal of physiology. Heart and circulatory physiology》2002,283(3):H983-H989
This study was undertaken to demonstrate the role of the RhoA/Rho kinase pathway in endothelin-1 (ET-1)-induced contraction of the rabbit basilar artery. Isometric tension and Western blot were used to examine ET-1-induced contraction and RhoA activation. The upstream effect on ET-1-induced RhoA activity was determined by using ET(A) and ET(B) receptor antagonists, protein kinase C (PKC), tyrosine kinase, and phosphatidylinositol-3 kinase inhibitors. The downstream effect of ET-1-induced contraction and RhoA activity was studied in the presence of the Rho kinase inhibitor Y-27632. The effect of Rho kinase inhibitor on ET-1-induced myosin light chain (MLC) phosphorylation was investigated by using urea-glycerol-PAGE immunoblotting. We found 1) ET-1 increased RhoA activity (membrane binding RhoA) in a concentration-dependent manner; 2) ET(A), but not ET(B), receptor antagonist abolished the effect of ET-1 on RhoA activation; 3) phosphodylinositol-3 kinase inhibitor, but not PKC and tyrosine kinase inhibitors, reduced ET-1-induced RhoA activation; 4) Rho kinase inhibitor Y-27632 (10 microM) inhibited ET-1-induced contraction; and 5) ET-1 increased the level of MLC phosphorylation. Rho kinase inhibitor Y-27632 reduced the effect of ET-1 on MLC phosphorylation. This study demonstrated that RhoA/Rho kinase activation is involved in ET-1-induced contraction in the rabbit basilar artery. Phosphodylinositol-3 kinase and MLC might be the upstream and downstream factors of RhoA activation. 相似文献
59.
Yimin Dai Qingfeng Zhou Chengwen Zhang Yanhua Song Xiaoyan Tian Xiangbin Zhang Chunyi Xue Shun Xu Yingzuo Bi Yongchang Cao 《Journal of virology》2012,86(22):12456
Porcine orthoreoviruses belong to the family Reoviridae and cause mainly mild enteritis in piglets. We present here the complete genome sequence of a novel porcine orthoreovirus strain (GD-1) isolated from a piglet in southern China. Our data will facilitate future investigations of the molecular characteristics and epidemiology of porcine orthoreoviruses. 相似文献
60.
Jiaomeng Pan Zhen Xiang Qingqiang Dai Zhenqiang Wang Bingya Liu Chen Li 《Journal of cellular biochemistry》2019,120(8):13478-13486
Lack of guidelines for personalized chemotherapy treatment after surgery has caused gastric cancer (GC) patients' unnecessary exposure to toxicity and the financial burden of chemotherapy treatments. In our study, we aimed to identify potential biomarkers to predict GC patients' susceptibility to platinum-based on Gene Expression Omnibus (GEO) data sets. A total of 603 differentially expressed genes (DEGs) were identified between platinum-resistant cell lines and platinum-sensitive cell lines based on the Cancer Cell Line Encyclopedia (CCLE) data sets. A total of 253 patients who had accepted radical gastrectomy were recruited, of which 97 received platinum-based chemotherapy and 156 were untreated. Three biomarkers (BRMS1, ND6, SRXN1) were then selected by univariate and multivariate Cox regression analysis to establish the predictive models using nomogram. Then this model was further validated through the GEO data set (GSE62254) which showed that this model could precisely predict the disease-free survival and overall survival of patients treated with platinum-based chemotherapy after surgery compared with untreated GC patients (P < 0.0001). This predictive model might provide helpful messages about the patients' susceptibility to platinum to guide personalized chemotherapy. 相似文献