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61.
氟离子选择电极法测啤酒中的氟   总被引:1,自引:0,他引:1  
本文采用氟离子电极法测定啤酒中的氟 ,测量溶液的酸度为PH5— 6,用总离子强度调节缓冲液 ,消除干扰离子及酸度的影响 ,方法回收率 96.1 2 %~ 99.2 4 % ,线性范围为 1 0 - 1 mol/L~ 5× 1 0 - 7mol/L ,最低检出浓度 0 .0 1 μg/ml,本法操作简单、快速 ,适合作常规测定 .  相似文献   
62.
报道了《河南植物志》中未记录的虎耳草科植物9种5变种(均采有标本)。  相似文献   
63.
Although techniques are available for the determination of the three-dimensional structure of biological specimens, for example scanning electron microscopy, they all have some serious drawback, such as low resolution, the requirement for crystals or for the sample to be analysed in a high vacuum. In an attempt to develop a technique for high-resolution three-dimensional structure analysis of non-crystalline biological material, we have tested the applicability of scanning tunnelling microscopy (STM), a method that has been used successfully in the analysis of metal and semiconductor surface structures. We report here that scanning tunnelling electron microscopy can be used to determine the surface topography of biological specimens at atmospheric pressure and room temperature, giving a vertical resolution of the order of 1 A. Our results show that quantum mechanical tunnelling of electrons through biological material is possible provided that the specimen is deposited on a conducting surface.  相似文献   
64.
说课是对教师的一个较高的要求,怎样上好一门课程,怎样清楚和完整地把说课的依据、内容和重点表述出来,是一个值得研究的问题。本文就说课方面的一些体会和收获进行了一些说明。  相似文献   
65.
A series of pharmacological and physiological studies have demonstrated the functional cross-regulation between MOR and NMDAR. These receptors coexist at postsynaptic sites in midbrain periaqueductal grey (PAG) neurons, an area implicated in the analgesic effects of opioids like morphine. In this study, we found that the MOR-associated histidine triad nucleotide-binding protein 1 (HINT1) is essential for maintaining the connection between the NMDAR and MOR. Morphine-induced analgesic tolerance is prevented and even rescued by inhibiting PKC or by antagonizing NMDAR. However, in the absence of HINT1, the MOR becomes supersensitive to morphine before suffering a profound and lasting desensitization that is refractory to PKC inhibition or NMDAR antagonism. Thus, HINT1 emerges as a key protein that is critical for sustaining NMDAR-mediated regulation of MOR signaling strength. Thus, HINT1 deficiency may contribute to opioid-intractable pain syndromes by causing long-term MOR desensitization via mechanisms independent of NMDAR.  相似文献   
66.
光学头定位控制由于快速性的要求使得系统产生振荡,影响定位精度.本文应用输入成形方法抑制光头在定位时的振动.通过建立光学头机电系统的数学模型,对于无参数摄动和有参数摄动两种情形分别应用零振荡()和零振荡加微分()两种输入成形控制器进行振动抑制,计算机数值仿真结果表明,该方法对于抑制光学头定位过程中的振动具有较好的效果.  相似文献   
67.
市政工程管线综合设计概述   总被引:2,自引:0,他引:2  
市政工程施工中,由于管线相碰,造成一系列经济及社会问题,遵循市政管线综合规划设计原则,进行合理的专业规划设计,能带来良好的经济及社会效益.  相似文献   
68.
The sheddase activity of ADAM17/TACE is regulated by the tetraspanin CD9   总被引:1,自引:1,他引:0  
ADAM17/TACE is a metalloproteinase responsible for the shedding of the proinflammatory cytokine TNF-α and many other cell surface proteins involved in development, cell adhesion, migration, differentiation, and proliferation. Despite the important biological function of ADAM17, the mechanisms of regulation of its metalloproteinase activity remain largely unknown. We report here that the tetraspanin CD9 and ADAM17 partially co-localize on the surface of endothelial and monocytic cells. In situ proximity ligation, co-immunoprecipitation, crosslinking, and pull-down experiments collectively demonstrate a direct association between these molecules. Functional studies reveal that treatment with CD9-specific antibodies or neoexpression of CD9 exert negative regulatory effects on ADAM17 sheddase activity. Conversely, CD9 silencing increased the activity of ADAM17 against its substrates TNF-α and ICAM-1. Taken together, our results show that CD9 associates with ADAM17 and, through this interaction, negatively regulates the sheddase activity of ADAM17.  相似文献   
69.
采用问卷调查的方法,对某大学本部除大四以外的在校本科生逃课现象进行调查研究。结果显示,大学生逃课现象较为普遍,且因年级、课程类型、上课时段以及班级人数等的不同而表现出差异性,这与学生缺乏自制力和明确的学习目标、学生对课程不感兴趣、课外活动冲击课堂教学以及社会功利风气有关。建议学校和任课教师加强学生思想政治教育、制度的建设与执行、学风建设以及课程教学改革等,解决和改善学生的逃课问题。  相似文献   
70.
Mutations affecting ciliary components cause ciliopathies. As described here, we investigated Tectonic1 (Tctn1), a regulator of mouse Hedgehog signaling, and found that it is essential for ciliogenesis in some, but not all, tissues. Cell types that do not require Tctn1 for ciliogenesis require it to localize select membrane-associated proteins to the cilium, including Arl13b, AC3, Smoothened and Pkd2. Tctn1 forms a complex with multiple ciliopathy proteins associated with Meckel and Joubert syndromes, including Mks1, Tmem216, Tmem67, Cep290, B9d1, Tctn2 and Cc2d2a. Components of this complex co-localize at the transition zone, a region between the basal body and ciliary axoneme. Like Tctn1, loss of Tctn2, Tmem67 or Cc2d2a causes tissue-specific defects in ciliogenesis and ciliary membrane composition. Consistent with a shared function for complex components, we identified a mutation in TCTN1 that causes Joubert syndrome. Thus, a transition zone complex of Meckel and Joubert syndrome proteins regulates ciliary assembly and trafficking, suggesting that transition zone dysfunction is the cause of these ciliopathies.  相似文献   
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