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71.
虽然表观遗传和衰老的关联性已经被广泛接受,但是两者之间内在的因果关系需要深度的理论阐述和分析.本文通过分析环境与表观遗传相互作用及其过程的本质特征,证明表观遗传记录多变的细胞环境和复杂的细胞事件是细胞的衰老之源.细胞周围环境以及所经历事件可通过表观修饰激活或抑制染色体上各个基因的表达,从而对染色体模板以及基因表达模式进行塑造.外在环境和细胞历史的多变性以及内在冲突性由此被逐渐记录在染色体模板上,整体上导致染色体模板以及基因表达模式的混乱和耗散.这将导致细胞表观熵(类似于Shannon信息熵)不可避免地逐渐衰减,其混乱度可通过细胞分裂而进一步被稳定积累、记忆和扩增.另外,表观修饰应对外在环境的变化存在滞后性和一定的不可逆性,加剧了表观熵的衰退. 相似文献
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酸雨对植物的危害,已为人们所共识.通过人工模拟酸雨实验,可进一步探讨酸雨 的低PH值(PH值由7.0下降到2.0)会使植物的叶细胞透性增加(叶细胞透性增加的百分率( %):青菜最大可达到214.2%,莴苣可达到136.23%).同时也会使植物叶片中的叶绿素含量 下降(青菜的叶绿素含量从0.851mg/g·鲜重下降到0.247mg/g·鲜重,莴苣的叶绿素含量从 0.868mg/g·鲜重下降到0.185mg/g·鲜重).进而影响植物的生长发育,对植物造成伤害. 相似文献
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INTRODUCTION Cell encapsulation in biocompatible and semipermeable polymeric membranes is an effective method for immunoprotection, regardless of the type of recipient (allograft, xenograft, etc.). The semipermeable nature of the membrane prevents high molecular weight molecules, antibodies and other immunologic moieties from coming into contact with the encapsulated cells and destroying them as foreign invaders, but permits the entry of nutrients and oxy- gen and the exit of therapeutic p… 相似文献
76.
Objective: To observe the effect of Yangxueqingnao particles on rat vascular smooth muscle cell (VSMC) proliferation induced
by lysophosphatidic acid (LPA). Methods: The amount of3H-TdR (3H-thymidine) admixed in cultured rat VSMC was measured and mitogen-activated protein kinase (MAPK) activity and lipid peroxidation
end product malondialdehyde (MDA) content of the VSMC were assayed. Results: 1×10−9, 1×10−8, 1×10−7 mol/L LPA in a concentration dependent manner, induced the amount of3H-TdR admixed, MAP kinase activity, and MDA content of the cultured rat VSMC to increase. However, 5%, 10%, and 15% Yangxueqingnao
serum preincubation resulted in a decrease of 23.0%, 42.0%, and 52.0% (P<0.01) respectively in the amount of3H-TdR admixed, a decline in VSMC MAP kinase activity of 13.9% (P<0.05), 29.6% (P<0.01), and 48.9% (P<0.01) respectively, and also, a decrease in MDA content of VSMC of 19.4%, 24.7%, and 43.2% (P<0.01) respectively, in the 1×10−7 mol/L LPA-treated VSMC. Conclusions: LPA activates the proliferation and lipid peroxidation of VSMC in a concentration dependent
manner. The LPA-induced VSMC proliferation is related to the activity of MAP kinases, enzymes involved in an intracellular
signalling pathway. The results of the present study showed that Yangxueqingnao particles can effectively inhibit LPA-induced
VSMC proliferation, MAP kinase activation, and reduce lipid peroxidative lesion.
Project (No. 491010-W50339) supported by Chinese Traditional Medicine Administration Bureau of Zhejiang Province, China 相似文献
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本文叙述了六倍体小偃麦与普通小麦杂交的细胞遗传研究,国内外技术的现状和发展趋势及目的、意义、理论和经济价值。 相似文献
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讨论了Daniell电池的热力学可逆性问题和电化学反应的判据问题,认为Daniell电池是热力学不可逆电池,电化学反应的ΔrGm判据与E判据并不等价。 相似文献
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Qi Ke Rui-na Yang Feng Ye Yu-jia Wang Qiong Wu Li Li Hong Bu 《Journal of Zhejiang University. Science. B》2012,13(9):695-706
Background and objective: Liver regeneration is a complex process regulated by a group of genetic and epigenetic factors. A variety of genetic factors have been reported, whereas few investigations have focused on epigenetic regulation during liver regeneration. In the present study, valproic acid (VPA), a histone deacetylase (HDAC) inhibitor, was used to investigate the effect of HDAC on liver regeneration. Methods: VPA was administered via intraperitoneal injection to 2/3 partially hepatectomized mice to detect hepatocyte proliferation during liver regeneration. The mice were sacrificed, and their liver tissues were harvested at sequential time points from 0 to 168 h after treatment. DNA synthesis was detected via a BrdU assay, and cell proliferation was tested using Ki-67. The expressions of cyclin D1, cyclin E, cyclin dependent kinase 2 (CDK2), and CDK4 were detected by Western blot analysis. Chromatin immunoprecipitation (ChIP) assay was used to examine the recruitment of HDACs to the target promoter regions and the expression of the target gene was detected by Western blot. Results: Immunohistochemical analysis showed that cells positive for BrdU and Ki-67 decreased, and the peak of BrdU was delayed in the VPA-administered mice. Consistently, cyclin D1 expression was also delayed. We identified B-myc as a target gene of HDACs by complementary DNA (cDNA) microarray. The expression of B-myc increased in the VPA-administered mice after hepatectomy (PH). The ChIP assay confirmed the presence of HDACs at the B-myc promoter. Conclusions: HDAC activities are essential for liver regeneration. Inhibiting HDAC activities delays liver regeneration and induces liver cell cycle arrest, thereby causing an anti-proliferative effect on liver regeneration. 相似文献