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Institution

Binzhou Medical College

EducationYantai, China
About: Binzhou Medical College is a education organization based out in Yantai, China. It is known for research contribution in the topics: Apoptosis & Cancer. The organization has 959 authors who have published 619 publications receiving 7642 citations.
Topics: Apoptosis, Cancer, Cell growth, Metastasis, Genotype


Papers
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Journal ArticleDOI
TL;DR: In the secondary prevention of stroke, platelet function measured with the continuous platelet counting method is closely related to recurrent ischemic vascular events; thus, this parameter has a good predictive value for recurrent ischemic vascular events.
Journal ArticleDOI
TL;DR: Results suggested that the anticancer effects of Euphorbiaceae extract may be involved in apoptosis induction, proliferation suppression, and oxidant scavenging.
Abstract: Background: As a promising means, natural products from Chinese herb provide valuable sources for cancer therapy. Euphorbiaceae has been used as a remedy for the treatment of many diseases, including cancer. However, studies about its effects on lung cancer are limited, and the mechanisms are not well established. Objective: The present study aims to investigate the anticancer effects of Euphorbiaceae extract (EE) in vitro and in vivo, as well as the potential mechanisms. Materials and Methods: In the present study, 3-(4,5-dimethythiazol-. 2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay was performed to investigate the effects of EE on Lewis lung adenocarcinoma cell (LLC) viability. Flow cytometric analysis was used to observe the changes of apoptosis and cell cycle of large cell carcinoma (LCC). The gene expressions were detected by real-time reverse transcription–polymerase chain reaction and Western blot. The tumorigenicity assay was performed to evaluate the inhibitory effects of EE in vivo. The activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) were also determined. Results: MTT assay demonstrated that EE significantly inhibited the growth of LLC in a dose-dependent manner in vitro. Flow cytometric analysis revealed that EE markedly induced apoptosis and G0/G1 arrest of the LCC cells. Furthermore, we found that EE led to the expression changes of apoptosis-related genes, with the decrease of Bcl-2 and the increase of Bax and caspase-9. The results from tumor-bearing animals further confirmed that the administration of EE significantly suppressed the tumor growth in vivo. Meanwhile, the activities of serum SOD, CAT, and GSH-Px increased significantly after the treatment of EE. Conclusion: These results suggested that the anticancer effects of EE may be involved in apoptosis induction, proliferation suppression, and oxidant scavenging.
Journal Article
25 Jan 2013-Tumori
TL;DR: Lentivirus-mediated shRNA targeting HOXA9 can steadily silence the expression of HOX a9 gene and enhance the drug sensitivity of U937 cells.
Abstract: Objective: To investigate the effect of lentivirus-mediated shRNA (short hairpin RNA) silencing HOXA9 (homeobox A9) gene on drug sensitivity of human acute monocytic leukemia U937 cells. Methods: RNAi (RNA interference) using a plasmid construct expressing shRNA targeting HOXA9 was detected by Western blotting. The plasmid expressing shRNA with highest level of knockdown was determined from four different plasmids and it was used to construct lentiviral vector HOXA9/GV118RNAi-LV#2. In this experiment, three groups were designed: control (without lentivirus infection), negative control (infected with negative lentivirus) and knockdown (infected with lentivirus containing shRNA targeting HOXA9) groups. After U937 cells were infected with HOXA9/GV118RNAi-LV#2, the silence efficiency was examined by real-time fluorogenic quantitative PCR, and the expression of HOXA9 protein was detected by Western blotting. The sensitivity of U937 cells to VCR (vincristine)/DNR (daunorubicin) after lentivirus infection was detected by MTT assay, and the apoptosis rate of U937 cells was detected by flow cytometry. The expression of MDR 1 (multidrug resistance protein 1) mRNA after DNR treatment in each group was determined by RT-PCR. Results: The silence efficiency of lentivirus-mediated shRNA targeting HOXA9 in U937 cells was more than or equal to 55% in knockdown group, and the expression level of HOXA9 protein was decreased obviously. The IC50 (half-maximal inhibitory concentration) values of VCR and DNR for U937 cells infected with HOXA9/GV118RNAi-LV#2 were significantly reduced (P < 0.01), and it revealed that the sensitivity to VCR/DNR was remarkably enhanced. The apoptosis rate of U937 cells in knockdown group was increased after VCR/DNR intervention (P < 0.01). The expression level of MDR 1 mRNA in U937 cells in knockdown group was significantly reduced after DNR intervention (P < 0.01). Conclusion: Lentivirus-mediated shRNA targeting HOXA9 can steadily silence the expression of HOXA9 gene and enhance the drug sensitivity of U937 cells. DOI:10.3781/j.issn.1000-7431.2013.01.004
Journal ArticleDOI
TL;DR: In the title solvated molecular salt, C28H28NO+·Cl−·C2H4O2, the central piperidinium ring of the cation adopts an envelope conformation with the N atom displaced by 0.798 (2) Å from the mean plane of the five C atoms.
Abstract: In the title solvated mol­ecular salt, C28H28NO+·Cl−·C2H4O2, the central piperidinium ring of the cation adopts an envelope conformation with the N atom displaced by 0.798 (2) A from the mean plane of the five C atoms. In the crystal, the components are linked by N—H⋯Cl and O—H⋯Cl hydrogen bonds into trimeric assemblies. C—H⋯Cl and C—H⋯π inter­actions further consolidate the packing.

Authors

Showing all 959 results

NameH-indexPapersCitations
Yuming Guo7349237180
Mingwen Zhao5536110884
Philip H.-S. Jen301373644
Qiusheng Zheng281172352
Qiang Fu19621094
Haixia Zhang17381155
Ling-Qun Kong1520931
Xuemei Hu1430395
Jichun Han1428447
Bao-guang Hu1120732
Xianbing Liu1121301
Xiaoyan Xu1015260
Yongfeng Gong1010521
Jingjing Xie1013457
Xiling Sun1018404
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20223
202136
202039
201932
201824
201739