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低基液氨质量分数对卡琳娜循环系统(kcs-34)理论循环效率的影响 被引量:8
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作者 任慧琴 李惟毅 张军朋 《机械工程学报》 EI CAS CSCD 北大核心 2012年第24期152-157,共6页
为探究卡琳娜循环系统(kcs-34)的热源进出口温度及质量流量均不发生变化的情况下,低基液氨质量分数a(<0.66)的变化对系统理论循环效率η的影响。通过改变蒸发器工质侧进口温度T8和富氨蒸气氨质量分数b,得出系统理论循环效率η与低基... 为探究卡琳娜循环系统(kcs-34)的热源进出口温度及质量流量均不发生变化的情况下,低基液氨质量分数a(<0.66)的变化对系统理论循环效率η的影响。通过改变蒸发器工质侧进口温度T8和富氨蒸气氨质量分数b,得出系统理论循环效率η与低基液氨质量分数a之间的关系。结果表明,在b不变的情况下,随着T8的增大,系统最大理论循环效率ηmax增大,a的取值区间呈减小趋势;在T8不变的情况下,随着b的增大,系统最大理论循环效率ηmax增大,系统最大理论循环效率ηmax对应的a值也逐渐增大,并且a的取值区间也呈增大趋势,同时,当T8保持不变并且a<0.36时,系统理论循环效率η会随着b的增大而减小,而当a>0.4时,系统理论循环效率η则会随着b的增大而增大。 展开更多
关键词 卡琳娜循环系统(kcs-34) 理论循环效率 氨-水溶液 低基液氨质量分数
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变温热源不可逆KCS-34循环的有限时间热力学优化 被引量:1
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作者 秦宛旭 秦晓勇 +1 位作者 陈林根 夏少军 《节能》 2018年第5期69-74,共6页
应用有限时间热力学理论建立了变温热源不可逆KCS-34循环模型,该模型考虑了热源和内部循环工质之间的传热热阻、膨胀机和循环泵的不可逆性、有限热容率热源和有限换热面积;分析了循环工质质量流率、蒸发器出口循环工质干度和冷凝器换热... 应用有限时间热力学理论建立了变温热源不可逆KCS-34循环模型,该模型考虑了热源和内部循环工质之间的传热热阻、膨胀机和循环泵的不可逆性、有限热容率热源和有限换热面积;分析了循环工质质量流率、蒸发器出口循环工质干度和冷凝器换热面积比对循环净功率、效率的影响,得到了循环净功率和热效率之间的关系;发现在各部件换热面积一定时,存在最佳的蒸发器出口循环工质干度使得循环效率最大,存在最佳的循环工质质量流率使得循环净功率最大;在蒸发器和冷凝器换热面积变化而总换热面积一定时,存在最佳的冷凝器换热面积比分别使得循环净功率或效率最大。所得结果对KCS-34循环的优化设计有一定的指导意义。 展开更多
关键词 有限时间热力学 不可逆循环 kcs-34循环 效率 净功率
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不可逆变温热源KCS-34循环生态学性能优化
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作者 秦宛旭 戈延林 +2 位作者 陈林根 秦晓勇 夏少军 《电力与能源》 2018年第5期652-657,共6页
应用有限时间热力学理论,基于变温热源不可逆KCS-34循环模型,分析了循环工质氨浓度变化时,循环工质质量流率和蒸发器出口循环工质干度对生态学函数的影响,并对循环净功率、效率与生态学函数三者之间的关系进行了对比分析。研究发现,当... 应用有限时间热力学理论,基于变温热源不可逆KCS-34循环模型,分析了循环工质氨浓度变化时,循环工质质量流率和蒸发器出口循环工质干度对生态学函数的影响,并对循环净功率、效率与生态学函数三者之间的关系进行了对比分析。研究发现,当以循环工质质量流率为变量时,生态学函数与效率、循环净功率与效率均呈类抛物线关系,而生态学函数与循环净功率之间关系曲线为扭叶型;当以蒸发器出口循环工质干度为变量时,循环净功率、效率和生态学函数任意两者之间的曲线关系均为扭叶型。 展开更多
关键词 有限时间热力学 kcs-34循环 生态学函数
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Influence of the Calmodulin Antagonist EBB on Cyclin B1 and Cdc2-p34 in Human Drug-resistant Breast Cancer MCF-7/ADR Cells
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作者 Xu Shi Yanhong Cheng Linglin Zou Dongsheng Xiong Yuan Zhou Ming Yang Dongmei Fan Xiaohua Dai Chunzheng Yang Huifang Zhu 《Chinese Journal of Clinical Oncology》 CSCD 2008年第2期108-112,共5页
OBJECTIVE To investigate the influence of O-(4-ethoxyl-butyl)- berbamine(EBB)on the expression of cyclin B1 and cdc2-p34 in the human drug-resistant breast cancer MCF-7/ADR cell line. METHODS The MTT assay was used to... OBJECTIVE To investigate the influence of O-(4-ethoxyl-butyl)- berbamine(EBB)on the expression of cyclin B1 and cdc2-p34 in the human drug-resistant breast cancer MCF-7/ADR cell line. METHODS The MTT assay was used to assess the cytotoxicity of EBB.Different levels of EBB were added to different cell lines at series of time points solely or combined with doxorubicin(DOX) to detect the effect on the expression of cyclinB1 and cdc2-p34 by Western blots.cdc2-p34 tyrosine phosphorylation was detected by immunoprecipitation.In addition,apoptosis and cytoplastic Ca 2+ concentrations were systematically examined by laser scanning confocal microscopy(LSCM). RESULTS EBB showed little inhibitory activity on human umbilical vein endothelial cells(ECV304),whereas EBB inhibited cell growth(IC50 range,4.55~15.74μmol/L)in a variety of sensitive and drug-resistance cell lines.EBB also down-regulated the expression of cyclin B1 and cdc2-p34 in a concentration and time dependent manner,which was an important reason for the G2/M phase arrest.EBB was shown to induce apoptosis of MCF-7/ADR cells while increasing the level of cytoplastic Ca 2+ . CONCLUSION The low cytotoxicity of EBB suggests it may be useful as a rational reversal agent.The effect of EBB on cell cycle arrest and related proteins,apoptosis,and cytoplastic Ca 2+ concentration may be involved in reversing multidrug resistance. 展开更多
关键词 EBB cell cycle cyclINB1 cdc2-p34 apoptosis Ca^2+.
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抑癌基因p53调控的微RNA——miR-34基因家族
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作者 陈雪 李子坚 +1 位作者 李力力 曹亚 《生命的化学》 CAS CSCD 北大核心 2008年第5期544-548,共5页
微RNA(microRNA,miRNA)是一种内源性非编码小RNA,在转录后水平调控基因表达,在肿瘤的发生发展过程中起重要作用。p53是重要的抑癌基因,在DNA损伤和癌基因等刺激下活化,诱导下游基因表达,使细胞周期阻滞、DNA修复并促进细胞衰老或凋亡。... 微RNA(microRNA,miRNA)是一种内源性非编码小RNA,在转录后水平调控基因表达,在肿瘤的发生发展过程中起重要作用。p53是重要的抑癌基因,在DNA损伤和癌基因等刺激下活化,诱导下游基因表达,使细胞周期阻滞、DNA修复并促进细胞衰老或凋亡。本文主要介绍近期发现的直接受p53调控的miR-34基因家族,及其在生长阻滞和细胞凋亡方面的研究进展,揭示了蛋白质与非编码RNA在重要的p53抑癌网络中的相互关系,为肿瘤的研究提供了新的思路。 展开更多
关键词 P53 miR-34 细胞周期 细胞凋亡
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Regulation Effect of miR-34a Expression on Radiosensitivity of Lung Adenocarcinoma Cells by Targeting Bcl-2 and CDK4/6 Signaling Pathways 被引量:1
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作者 Xue Chen Chen Yin +1 位作者 Qingfen Liu Jianxiang Liu 《Journal of Cancer Therapy》 2022年第4期187-198,共12页
Objective: Radiotherapy has been widely used to treat lung cancer. However, non-small lung cancer cells are insensitive to radiation, diminishing their radiotherapy effects. Although the radiosensitivity of the non-sm... Objective: Radiotherapy has been widely used to treat lung cancer. However, non-small lung cancer cells are insensitive to radiation, diminishing their radiotherapy effects. Although the radiosensitivity of the non-small lung cancer cells was reported to be enhanced through regulating miR-34a, the regulation effects of miR-34a expression on radiosensitivity of lung adenocarcinoma cells through target genes CDK4, CDK6, CyclinD1, and Bcl-2/Bax have not been systematically investigated. Methods: In this study, we investigated the effect of miR-34a expression on the Bcl-2, CDK4, and CDK6 pathways in lung adenocarcinoma cells, to provide new insights into the sensitization treatment of lung cancer. We first studied the effect of miR-34a expression on H1299 and A549 cell activity. Then to investigate the mechanisms of radiosensitivity, we focused on apoptosis, cell cycle, and target genes. Results: We find that overexpression of miR-34a in lung adenocarcinoma cells inhibits cell activity, and improves radiosensitivity. Specifically, overexpression of miR-34a suppresses the expression of target genes CDK4, CDK6, CyclinD1, and Bcl-2/Bax, which leads to cell cycle arrest and promotes apoptosis of lung adenocarcinoma cells. Conclusions: Overall, our results demonstrate that the overexpression of miR-34a enhances the radiosensitivity of lung adenocarcinoma cells, indicating that miR-34a is a sensitizer for lung adenocarcinoma radiotherapy. 展开更多
关键词 MIR-34A p53 Lung Adenocarcinoma Cells RADIOSENSITIVITY Cell Apoptosis Cell cycle
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Bifurcation of limit cycles near equivariant compound cycles 被引量:1
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作者 Mao-an HAN Tong-hua ZHANG Hong ZANG 《Science China Mathematics》 SCIE 2007年第4期503-514,共12页
In this paper we study some equivariant systems on the plane. We first give some criteria for the outer or inner stability of compound cycles of these systems. Then we investigate the number of limit cycles which appe... In this paper we study some equivariant systems on the plane. We first give some criteria for the outer or inner stability of compound cycles of these systems. Then we investigate the number of limit cycles which appear near a compound cycle of a Hamiltonian equivariant system under equivariant perturbations. In the last part of the paper we present an application of our general theory to show that a Z3 equivariant system can have 13 limit cycles. 展开更多
关键词 equivariant system STABILITY BIFURCATION limit cycle 34C05 34G10 58F11
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On the limit cycles of a quintic planar vector field
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作者 Yu-hai WU Li-xin TIAN Mao-an HAN 《Science China Mathematics》 SCIE 2007年第7期925-940,共16页
This paper concerns the number and distributions of limit cycles in a Z 2-equivariant quintic planar vector field. 25 limit cycles are found in this special planar polynomial system and four different configurations o... This paper concerns the number and distributions of limit cycles in a Z 2-equivariant quintic planar vector field. 25 limit cycles are found in this special planar polynomial system and four different configurations of these limit cycles are also given by using the methods of the bifurcation theory and the qualitative analysis of the differential equation. It can be concluded that H(5) ? 25 = 52, where H(5) is the Hilbert number for quintic polynomial systems. The results obtained are useful to study the weakened 16th Hilbert problem. 展开更多
关键词 double homoclinic loop Melnikov function STABILITY BIFURCATION limit cycles CONFIGURATION 34C07 34C23 34C37 37G15
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Effect of Allitridi on Inducing Mitotic Arrest in Human Gastric Cell Line SGC-7901 and Its Possible Mechanism
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作者 陈铁军 哈敏文 +2 位作者 宫月华 徐倩 袁媛 《Chinese Journal of Cancer Research》 SCIE CAS CSCD 2008年第2期126-132,共7页
Objective: To learn the effect of allitridi on inducing mitotic arrest in human gastric cell line SGC-7901 and its possible mechanisms. Methods: We treated SGC-7901 cells with allitridi, and observed the proliferati... Objective: To learn the effect of allitridi on inducing mitotic arrest in human gastric cell line SGC-7901 and its possible mechanisms. Methods: We treated SGC-7901 cells with allitridi, and observed the proliferation inhibitory rate with MTT colometric assay, changes of cell cycle using flow cytometry and Switzerland-Giemsa's staining, and morphologic changes of the microtubule structure and location changes of cyclin BI expression using immunofluorescence and confocal laser scanning microscope. Furthermore, the expression of cyclin B1 was analyzed quantitatively using Leica confocal software. Results: SGC-7901 cells were inhibited after exposure to allitridi and the IC50 was 7.2μg/ml for 24 h, 20μg/ml for 72 h. When the cells were treated with allitridi at concentrations of 3, 6, and 9μg/ml for 24 h respectively, there was a declining tendency in the percentage of G0/G1 cell but an increasing tendency in GE/M cell in the allitridi treated group compared with that of control (P〈0.01). When cells were treated allitridi at concentration of 6 μg/ml for 24 h, its mitotic index was much higher (P〈0.01) than that of control, suggesting that allitridi caused arrest of gastric cancer cells in M phase. The cells were treated with allitridi became more shrunken and nepheloid, in which the microtubule networks disappeared, while the control cell exhibited an intact microtubule network. Contrasting with normal existence mainly in the cytoplasm, the cyclin B1 was expressed more significantly and concentrated in the nucleus after exposure to allitridi. Fluorescence intensity of cyclin B 1 protein in cells treated with allitridi was much more higher than that of control (P〈0.001). Conclusion: Allitridican induce arrest of SGC-7901 cells in M phase, probably through enhancing microtubule depolymerization by elevating the expression of cyclin B1. 展开更多
关键词 Allitridi Stomach neoplasms Cell cycle P34 cdc2/cyclin B1 MICROTUBULE
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ON  THE  NONEXISTENCE  OF  THE  LIMIT  CYCLEFOR  QUADRATIC  SYSTEM  OF  TYPE III
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作者 徐思林 《Annals of Differential Equations》 1999年第1期77-82,共6页
In tills paper, several new criteria on the nonexistence of limit cycles forquadratic system of Type III are given.
关键词 qlladratic system of Type III limit cycle nonexistenceAMS Subject Classification 34C05
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五味子乙素通过上调miR-34诱导肾癌细胞生长抑制、凋亡和细胞周期阻滞 被引量:2
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作者 方维 叶爱武 汪妮 《医学分子生物学杂志》 CAS 2020年第6期436-442,共7页
目的探讨五味子乙素对肾癌细胞生长和细胞周期的作用及机制方法将786-0细胞分为对照组、五味子乙素处理组(12.5、25、50 μmol/L)、阳性对照组(10μmol/L顺铂)、rmR-34 inhibitor组、50 μmol/L五味子乙素+miR-34 inhibitor组。MTT检测... 目的探讨五味子乙素对肾癌细胞生长和细胞周期的作用及机制方法将786-0细胞分为对照组、五味子乙素处理组(12.5、25、50 μmol/L)、阳性对照组(10μmol/L顺铂)、rmR-34 inhibitor组、50 μmol/L五味子乙素+miR-34 inhibitor组。MTT检测细胞增殖,克隆形成检测细胞生长,流式检测细胞凋亡率,流式细胞术检测细胞周期,Western印迹检测Ki67、PCNA、Bax、Bcl-2、Caspase-3、cyclin D1、CDK2和CDK4蛋白表达,RT-qPCR检测miR-34表达。结果五味子乙素抑制细胞增殖力、降低细胞克隆数目、提升细胞凋亡率、诱导G0/G1期分布(P<0.05、P<0.01),同时上调细胞中Bax、Caspase-3蛋白表达和miR-34 mRNA的表达,下调Ki67、PCNA、Bcl-2、cyclin D1、CDK2和CDK4蛋白表达(P<0.05、P<0.01);miR-34 inhibitor具有相反的作用,但五味子乙素可以削弱miR-34 inhibitor的作用。结论五味子乙素通过上调miR-34抑制肾癌细胞的生长、诱导其凋亡和周期阻滞。 展开更多
关键词 五味子乙素 miR-34 肾癌 生长 凋亡 细胞周期阻滞
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Increase of Calcium Levels at Interphase in NIH 3T3 Cells
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作者 薛绍白 张鸿卿 +1 位作者 成汝萱 李素文 《Science China Chemistry》 SCIE EI CAS 1993年第3期314-318,共5页
The fluorescent calcium ion indicator dye Fluo-3 and DNA-binding dye Hoechst 33342 were employed to determine, in a quantitative microspectrofluorometric study, the intracellular calcium ion concentration ([Ca^(2+)]_i... The fluorescent calcium ion indicator dye Fluo-3 and DNA-binding dye Hoechst 33342 were employed to determine, in a quantitative microspectrofluorometric study, the intracellular calcium ion concentration ([Ca^(2+)]_i) and the DNA content of individual living NIH3T3 cells. The well-separated excitation and emission properties of these dyes allowed us to establish for each cell both the phase of the cell cycle using DNA content and [Ca^(2+)]_i. We found that the transition from G_1, through S, to the G_2 phase is accompanied by a two-fold increase in [Ca^(2+)]_i. The [Ca^(2+)]_i was inhomologous in each phase of the interphase (G_1, S and G_2) although [Ca^(2+)]_i in the S and G_2 phases was never lower than certain threshold values in the G_1 and S phases respectively. [Ca^(2+)]_i in G_0 cells was lower than that in G_2 cells. These changes in [Ca^(2+)]_i suggest that [Ca^(2+)]_i may be an import regulator of cell cycle progression. 展开更多
关键词 intracellular calcium fluo-3 cell cycle Go cell p34^(cdex).
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