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921.
谷胱甘肽的抗线粒体脂质过氧化作用 总被引:2,自引:0,他引:2
谷胱甘肽是细胞内重要的抗氧化损伤物质之一.以NADH诱导的牛心肌线粒体脂质过氧化体系为模型,研究了谷胱甘肽的抗氧化作用.结果表明,一定浓度的谷胱甘肽能够部分抑制该体系中线粒体的脂质过氧化.保护组的丙二醛含量为损伤组72.5%;线粒体的膨胀度较损伤组降低;细胞色素C氧化酶及ATP酶活力分别较损伤组提高了1.5及2.2倍. 相似文献
922.
923.
Gao D Inuzuka H Tan MK Fukushima H Locasale JW Liu P Wan L Zhai B Chin YR Shaik S Lyssiotis CA Gygi SP Toker A Cantley LC Asara JM Harper JW Wei W 《Molecular cell》2011,44(2):290-303
The activities of both mTORC1 and mTORC2 are negatively regulated by their endogenous inhibitor, DEPTOR. As such, the abundance of DEPTOR is a critical determinant in the activity status of the mTOR network. DEPTOR stability is governed by the 26S-proteasome through a largely unknown mechanism. Here we describe an mTOR-dependent phosphorylation-driven pathway for DEPTOR destruction via SCF(βTrCP). DEPTOR phosphorylation by mTOR in response to growth signals, and in collaboration with casein kinase I (CKI), generates a phosphodegron that binds βTrCP. Failure to degrade DEPTOR through either degron mutation or βTrCP depletion leads to reduced mTOR activity, reduced S6 kinase activity, and activation of autophagy to reduce cell growth. This work expands the current understanding of mTOR regulation by revealing a positive feedback loop involving mTOR and CKI-dependent turnover of its inhibitor, DEPTOR, suggesting that misregulation of the DEPTOR destruction pathway might contribute to aberrant activation of mTOR in disease. 相似文献
924.
Simultaneous modification of three homoeologs of TaEDR1 by genome editing enhances powdery mildew resistance in wheat 下载免费PDF全文
Yunwei Zhang Yang Bai Guangheng Wu Shenghao Zou Yongfang Chen Caixia Gao Dingzhong Tang 《The Plant journal : for cell and molecular biology》2017,91(4):714-724
Wheat (Triticum aestivum L.) incurs significant yield losses from powdery mildew, a major fungal disease caused by Blumeria graminis f. sp. tritici (Bgt). enhanced disease resistance1 (EDR1) plays a negative role in the defense response against powdery mildew in Arabidopsis thaliana; however, the edr1 mutant does not show constitutively activated defense responses. This makes EDR1 an ideal target for approaches using new genome‐editing tools to improve resistance to powdery mildew. We cloned TaEDR1 from hexaploid wheat and found high similarity among the three homoeologs of EDR1. Knock‐down of TaEDR1 by virus‐induced gene silencing or RNA interference enhanced resistance to powdery mildew, indicating that TaEDR1 negatively regulates powdery mildew resistance in wheat. We used CRISPR/Cas9 technology to generate Taedr1 wheat plants by simultaneous modification of the three homoeologs of wheat EDR1. No off‐target mutations were detected in the Taedr1 mutant plants. The Taedr1 plants were resistant to powdery mildew and did not show mildew‐induced cell death. Our study represents the successful generation of a potentially valuable trait using genome‐editing technology in wheat and provides germplasm for disease resistance breeding. 相似文献
925.
为了探讨毛竹(Phyllostachys pubescens)茎秆的光合特性,以1龄和3龄毛竹为材料,观察了茎秆和叶中叶绿体的超微结构,测定了光合色素含量以及发射荧光光谱。结果表明:茎秆中叶绿体发育完整,其类囊体垛叠程度高于叶,并含有淀粉粒。茎秆中叶绿素总含量、类胡萝卜素及Chla/b含量显著低于叶(FI〈O.05)。茎秆发射荧光光谱在735nm处没有明显的主峰,1龄和3龄毛竹茎秆光系统lI与光系统I的半峰宽比值分别比叶降低了7.0%和11.3%(P〈0.05),峰高比值比叶分别增加了6.5%和18.3%(P〈0.05)。四阶导数光谱在650—800nm波长范围内出现了6个极大值,代表LHCII、CP43、CP47、RCI和ILHCI的发射荧光峰以及PSI和PSII的发射荧光副振峰:其中,茎秆中RCI和LHCI特征发射荧光峰与叶相比有不同程度的红移。表明毛竹茎秆叶绿体通过提高Chlb的相对含量和增加类囊体垛叠以及降低LHCI含量,来适应毛竹茎秆以红光为主的光环境。进而协调激发能在2个光系统间的分配。 相似文献
926.
Bidhan A. Shinkre T. Santhosh Kumar Zhan-Guo Gao Francesca Deflorian Kenneth A. Jacobson William C. Trenkle 《Bioorganic & medicinal chemistry letters》2010,20(19):5690-5694
Movement disorders such as Parkinson’s disease and Huntington’s disease are serious life-limiting and debilitating movement disorders. Their onset typically occurs from mid-life to late in life, and effective diagnostic techniques for detecting and following the disease course are lacking. Our goal is to develop receptor imaging agents for positron emission tomography (PET) that selectively target the most relevant subtype of adenosine receptors (AR) that are highly expressed in the striatum, that is, the A2A AR. To further this goal, we have synthesized and characterized pharmacologically a family of high affinity A2A AR ligands, based on the known antagonist, SCH 442416 (R = –Me), which have structural variability on the terminus (R = –Et, –i-Pr, –allyl, and others). A O-fluoroethyl analogue suitable for use as a PET tracer had a Ki value of 12.4 nM and was highly selective for the A2A AR in comparison to the A1 and A3 ARs. 相似文献
927.
Favre J Gao J Zhang AD Remy-Jouet I Ouvrard-Pascaud A Dautreaux B Escoubet B Thuillez C Jaisser F Richard V 《American journal of physiology. Heart and circulatory physiology》2011,300(6):H2035-H2043
The deleterious effects of aldosterone excess demonstrated in cardiovascular diseases might be linked in part to coronary vascular dysfunction. However, whether such vascular dysfunction is a cause or a consequence of the changes occurring in the cardiomyocytes is unclear. Moreover, the possible link between mineralocorticoid receptor (MR)-mediated effects on the cardiomyocyte and the coronary arteries is unknown. Thus we used a mouse model with conditional, cardiomyocyte-specific overexpression of human MR (hMR) and observed the effects on endothelial function in isolated coronary segments. hMR overexpression decreased the nitric oxide (NO)-mediated relaxing responses to acetylcholine in coronary arteries (but not in peripheral arteries), and this was prevented by a 1-mo treatment either with an MR antagonist, vitamin E/vitamin C, or a NADPH oxidase inhibitor. hMR overexpression did not affect coronary endothelial NO synthase content nor its level of phosphorylation on serine 1177, but increased cardiac levels of reactive oxygen species, cardiac NADPH oxidase (NOX) activity, and expression of the NOX subunit gp91phox, which was limited to endothelial cells. Thus an increase in hMR activation, restricted to cardiomyocytes, is sufficient to induce a severe coronary endothelial dysfunction. We suggest a new paracrine mechanism by which cardiomyocytes trigger a NOX-dependent, reactive oxygen species-mediated coronary endothelial dysfunction. 相似文献
928.
929.
Association between the change in body mass index from early adulthood to midlife and subsequent type 2 diabetes mellitus 下载免费PDF全文
Yiming Mu Chao Liu Jiajun Zhao Lulu Chen Qiang Li Tao Yang Li Yan Qin Wan Shengli Wu Yan Liu Guixia Wang Zuojie Luo Xulei Tang Gang Chen Yanan Huo Zhengnan Gao Qing Su Youmin Wang Guijun Qin Huacong Deng Xuefeng Yu Feixia Shen Li Chen Liebin Zhao Jichao Sun Lin Ding Yu Xu Min Xu Meng Dai Tiange Wang Di Zhang Jieli Lu Yufang Bi Shenghan Lai Donghui Li Weiqing Wang Guang Ning 《Obesity (Silver Spring, Md.)》2016,24(3):703-709
930.