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1.
18MeV质子辐照对Zr-Sn-Nb合金性能影响的研究 总被引:2,自引:1,他引:2
作者通过HZ B串列加速器用能量 18MeV的质子 ,研究了两种Zr Sn Nb合金的质子辐照效应 .结果表明 ,经 1.5× 10 14 /cm2 注量质子辐照处理后 ,其样品的电阻率升高 ,而显微组织没有明显的变化 .通过计算在此能量和注量下锆合金的初级撞出能量为 770keV ,足以产生级联碰撞 ,致使样品中的原子移位而生成点缺陷 ,从而电阻率上升 ,但因注量较小不能使显微组织发生明显的变化 相似文献
2.
PKA和PKC对HeLa细胞G2/M/G1进程的影响 总被引:2,自引:0,他引:2
为了研究PKA和PKC对HeLa细胞G2→用M→G1期进程的影响,用PKA和PKC抑制剂分别处理同步的G2期和M期的HeLa细胞后,测定了细胞有丝分裂指数和PKA,PKC与CDC2激酶的活性。 相似文献
3.
On the basis of evidence collected from the literature, we propose a general model by which protein kinase (PK) A and the
different PKC isoforms can inversely affect cell growth. Molecular switches, which are able to direct the signal towards antiproliferative
or mitogenic pathways, are the different isoforms of Raf and PKC. Conflicting data are also reported and discussed in an attempt
to reconcile them.
Received 10 November 2005; received after revision 28 December 2005; accepted 3 January 2006 相似文献
4.
Pancreatic cells express the proglucagon gene ( gcg ) and thereby produce the peptide hormone glucagon , which stimulates hepa tic glucose production and thereby increases blood glucose levels. The same gcg gene is also expressed in the intesti nal endocrine L cells and certain neural cells in the brain. In the gut, gcg expression leads to the production of glucagon-like peptide-1 (GLP-1). This incretin hormone stimulates insulin secretion when blood glucose, level is high. In addition, GLP-1 stimulates pancreatic cell proliferation, inhibits cell apoptosis, and has been utilized in the trans-differentiation of insulin producing cells. 相似文献
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细胞粘附分子gp150在盘基网柄菌细胞发育后期起着重要作用.用gp150抗体定位gp150在细胞发育重要阶段的分布,显示在细胞发育的不同时段,gp150的定位有着明显的区别.在聚集前的细胞流时期,gp150还均匀分布在细胞质内,到了细胞丘时期,gp150就移至多细胞聚集体的边缘部位.到了蛞蝓体时期,gp150在前柄细胞的表达量明显大于前孢子细胞,提示了gp150对柄细胞的作用.而当细胞发育至子实体阶段,gp150大量分布在成熟孢子的孢壁上,这是目前还没有报道的.高效液相色谱法检测野生型KAx-3细胞和gp150过表达细胞KAx-3:acct15/lagC的PKA活性,显示在细胞发育的早期(10 h之前),PKA在野生型细胞中的活性比KAx-3:act15/lagC细胞低.但是在细胞发育的后期,也就是野生型细胞中gp150开始快速积累之后,PKA在野生型细胞中的活性比KAx-3:act15/lagC细胞高.这些结果说明,gp150和PKA之间可能存在某种负反馈环的关系共同调节盘基网柄菌的生长发育. 相似文献
8.
ERKs are the point of divergence of PKA and PKC activation by PTHrP in human skin fibroblasts 总被引:3,自引:0,他引:3
Fortino V Torricelli C Gardi C Valacchi G Rossi Paccani S Maioli E 《Cellular and molecular life sciences : CMLS》2002,59(12):2165-2171
Parathyroid hormone-related peptide (PTHrP) receptors, coupled to trimeric G proteins, operate in most target cells through
at least three different transduction routes: Gαs-mediated stimulation of adenylylcyclase (AC), Gαq-mediated activation of
phospholipase Cβ (PLC) and mitogen-activated protein kinase (MAPK) activation. In this study we investigated the relative
role of different pathways in human skin fibroblast prolifera-tion. Using chemical inhibitors and activators of signal transduction,
we demonstrated that: (i) AC/cAMP and PLC/1,4,5 inositol triphosphate/diacylglycerol second-messenger systems are simultaneously
activated following PTHrP binding to its receptors; (ii) the mitogenic response to PTHrP derives from a balance between two
counteracting pathways – an activating route mediated by protein kinase C (PKC) and an inhibitory route mediated by protein
kinase A (PKA); (iii) PTHrP mitogenic effects are largely dependent on MAPKs, whose activity can be modulate
d by both PKA and PKC. Our results indicate that MAPKs are common targets of both transduction routes and, at the same time,
their point of divergence in mediating PTHrP dual and opposite mitogenic effects.
Received 2 August 2002; received after revision 10 September 2002; accepted 18 October 2002
RID="*"
ID="*"Corresponding author. 相似文献
9.
本文采用分子动力学方法模拟了不同初级离位原子(PKA)能量下单晶α锆的辐照损伤动态过程,以及辐照后的缺陷模型在沿[0001]单轴拉伸下的力学性能及微观结构演变。结果表明,随着PKA能量的增加,α锆晶体中辐照产生的Frenkel缺陷对数目稳步增加;单轴拉伸模拟结果显示,辐照产生的Frenkel缺陷对会显著降低单晶α锆的屈服强度,且随着PKA能量的增大,辐照材料的屈服强度呈缓慢逐渐下降的趋势;结合拉伸形变过程的微观结构演化可知,辐射产生的缺陷为位错环提供了成核位置,在较低的应变下即产生了大量位错,导致辐照后α锆的屈服强度大幅降低。 相似文献
10.
Ruminations on dietary restriction and aging 总被引:6,自引:0,他引:6
Kennedy BK Steffen KK Kaeberlein M 《Cellular and molecular life sciences : CMLS》2007,64(11):1323-1328
Calorie restriction has been known for many decades to extend the life span of rodents. Since the more recent discovery that
a long-term reduction in nutrient intake also extends life span in nearly every invertebrate model organism used for aging
research, the mechanisms behind the longevity benefits of this intervention have been under intense scrutiny. While models
have been developed in yeast, worms, and flies, the molecular mechanisms governing life span extension by calorie restriction
remain controversial, resulting in great anticipation of mammalian studies testing these models. Here we discuss the links
between nutrient reduction and enhanced longevity with emphasis on evolutionarily conserved nutrient response signaling.
Received 1 November 2006; received after revision 15 December 2006; accepted 27 February 2007 相似文献