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101.
探索新兴技术竞争优势的测度方法,有助于我们把握技术前沿的竞争态势,推动科技成果的转化。采用四象限图示分析方法和雷达图示分析方法,借助Relecura专业知识产权分析平台,以细胞免疫治疗为实证,对技术主体的综合竞争优势和高产机构在主要技术领域、子领域、IPC代码的竞争优势进行了分析。就专利技术战略布局的前瞻性指标而言,美国国立卫生研究院和美国卫生与公众服务部两个机构最具有前瞻性。就创造高价值专利的执行力而言,美国国立卫生研究院和Celera公司具有相对比较强的创造高价值专利技术的执行力。高产机构在主要技术领域的竞争优势各异,美国卫生与公众服务部在更多的技术子领域和IPC代码具有优势。 相似文献
102.
DNA-damage response network at the crossroads of cell-cycle checkpoints,cellular senescence and apoptosis 总被引:2,自引:0,他引:2
Schmitt E Paquet C Beauchemin M Bertrand R 《Journal of Zhejiang University. Science. B》2007,8(6):377-397
Tissue homeostasis requires a carefully-orchestrated balance between cell proliferation, cellular senescence and cell death. Cells proliferate through a cell cycle that is tightly regulated by cyclin-dependent kinase activities. Cellular senescence is a safeguard program limiting the proliferative competence of cells in living organisms. Apoptosis eliminates unwanted cells by the coordinated activity of gene products that regulate and effect cell death. The intimate link between the cell cycle, cellular senescence, apoptosis regulation, cancer development and tumor responses to cancer treatment has become eminently apparent. Extensive research on tumor suppressor genes, oncogenes, the cell cycle and apoptosis regulatory genes has revealed how the DNA damage-sensing and -signaling pathways, referred to as the DNA-damage response network, are tied to cell proliferation, cell-cycle arrest, cellular senescence and apoptosis. DNA-damage responses are complex, involving "sensor" proteins that sense the damage, and transmit signals to "transducer" proteins, which, in turn, convey the signals to numerous "effector" proteins implicated in specific cellular pathways, including DNA repair mechanisms, cell-cycle checkpoints, cellular senescence and apoptosis. The Bcl-2 family of proteins stands among "the mos"t crucial regula"tors of apop"tosis and performs vi"tal func"tions in deciding whether a cell will live or die after cancer chemotherapy and irradiation. In addition, several studies have now revealed that members of the Bcl-2 family also interface with the cell cycle, DNA repair/recombination and cellular senescence, effects that are generally distinct from their function in apoptosis. In this review, we report progress in understanding the molecular networks that regulate cell-cycle checkpoints, cellular senescence and apoptosis after DNA damage, and discuss the influence of some Bcl-2 family members on cell-cycle checkpoint regulation. 相似文献
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104.
Xu Q Li ZX Peng HQ Sun ZW Cheng RL Ye ZM Li WX 《Journal of Zhejiang University. Science. B》2011,12(4):247-255
This paper aims to investigate the effects of artesunate (ART) on growth and apoptosis in human osteosarcoma HOS cell line
in vitro and in vivo and to explore the possible underlying mechanisms. Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium
bromide (MTT) assay. The induction of apoptosis was detected by light and transmission electron microscopy and flow cytometry.
Western blot analysis was used to investigate the related mechanisms. Nude mice were further employed to investigate the antitumour
activity of ART in vivo. MTT assay results demonstrated that ART selectively inhibits the growth of HOS cells in a dose- and
time-dependent manner. Based on the findings of light and transmission electron microscopy, Hoechst 33258 staining, and fluorescein
isothiocyanate (FITC)-annexin V staining, the cytotoxicity of ART in HOS cells occurs through apoptosis. With ART treatment,
cytosolic cytochrome c was increased, Bax expression was gradually upregulated, Bcl-2 expression was downregulated, and caspase-9 and caspase-3
were activated. Thus, the intrinsic apoptotic pathway may be involved in ART-induced apoptosis. Cell cycle analysis by flow
cytometry indicated that ART may induce cell cycle arrest at G2/M phase. In nude mice bearing HOS xenograft tumours, ART inhibited tumour growth and regulated the expressions of cleaved
caspase-3 and survivin, in agreement with in vitro observations. ART has a selective antitumour activity against human osteosarcoma
HOS cells, which may be related to its effects on induction of apoptosis via the intrinsic pathway. The results suggest that
ART is a promising candidate for the treatment of osteosarcoma. 相似文献
105.
BackgroundButyrate is a histone deacetylase inhibitor that induces apoptosis and inhibits cell proliferation of colorectal cancer cells. To improve its anticancer activity, butyrate has been evaluated mixed with drugs and different molecules. Plant antimicrobial peptides are attractive anticancer alternative molecules because they show selective cytotoxic activity against different cancer cell lines. In this work, we explore if the plant defensin γ-thionin (Capsicum chinense) can improve butyrate activity on Caco-2 cell line and we also determined the mechanism of death activated.ResultsThe combined treatment of γ-thionin (3.5 µM) and butyrate (50 mM) showed higher cytotoxicity on Caco-2 cells with respect to single treatments. Also, the combined treatment reduced cell proliferation and exhibited a higher rate of apoptosis than single treatments. Combined treatment induced caspases 8 and 9 activation to an extent comparable with that of butyrate while γ-thionin did not activate caspases. Additionally, reactive oxygen species generation preceded the onset of apoptosis, and superoxide anion production was higher in cells treated with the combined treatment.ConclusionsThe γ-thionin from Habanero chili pepper improved the butyrate cytotoxicity on Caco-2 cells. This effect occurred through apoptosis induction associated with reactive oxygen species production. Therefore, the combination of butyrate with cytotoxic antimicrobial peptides could be an attractive strategy for cancer therapy.How to cite: Velázquez-Hernández ME, Ochoa-Zarzosa A, López-Meza JE, Defensin γ-thionin from Capsicum chinense improves butyrate cytotoxicity on human colon adenocarcinoma cell line Caco-2. Electron J Biotechnol 2021;52. https://doi.org/10.1016/j.ejbt.2021.04.009 相似文献
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107.
The paper studies the dynamics of production of knowledge in an emergent scientific field, Nanoscience. It suggests that scientific knowledge advances by proliferation, or the turbulent entry of new sub-fields, each generating opportunities for further entries at each time. It suggests a new methodology to define and measure the dynamics of knowledge, based on the industrial dynamics of keywords and a formal representation through bipartite graphs. An empirical examination of the graph dynamics in the early stage of the scientific field (1988-2002) confirms the notion of proliferation. 相似文献
108.
Zhaoshi BAI Yaling PENG Xinyue YE Zhixian LIU Yupeng LI Lingman MA 《Journal of Zhejiang University. Science. B》2022,23(2):89
Cancer is the leading cause of death worldwide. Drugs play a pivotal role in cancer treatment, but the complex biological processes of cancer cells seriously limit the efficacy of various anticancer drugs. Autophagy, a self-degradative system that maintains cellular homeostasis, universally operates under normal and stress conditions in cancer cells. The roles of autophagy in cancer treatment are still controversial because both stimulation and inhibition of autophagy have been reported to enhance the effects of anticancer drugs. Thus, the important question arises as to whether we should try to strengthen or suppress autophagy during cancer therapy. Currently, autophagy can be divided into four main forms according to its different functions during cancer treatment: cytoprotective (cell survival), cytotoxic (cell death), cytostatic (growth arrest), and nonprotective (no contribution to cell death or survival). In addition, various cell death modes, such as apoptosis, necrosis, ferroptosis, senescence, and mitotic catastrophe, all contribute to the anticancer effects of drugs. The interaction between autophagy and these cell death modes is complex and can lead to anticancer drugs having different or even completely opposite effects on treatment. Therefore, it is important to understand the underlying contexts in which autophagy inhibition or activation will be beneficial or detrimental. That is, appropriate therapeutic strategies should be adopted in light of the different functions of autophagy. This review provides an overview of recent insights into the evolving relationship between autophagy and cancer treatment. 相似文献
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