首页 | 本学科首页   官方微博 | 高级检索  
文章检索
  按 检索   检索词:      
出版年份:   被引次数:   他引次数: 提示:输入*表示无穷大
  收费全文   21428篇
  免费   1500篇
  国内免费   28篇
  2024年   27篇
  2023年   69篇
  2022年   243篇
  2021年   415篇
  2020年   249篇
  2019年   312篇
  2018年   531篇
  2017年   394篇
  2016年   684篇
  2015年   1131篇
  2014年   1229篇
  2013年   1398篇
  2012年   1834篇
  2011年   1714篇
  2010年   1101篇
  2009年   917篇
  2008年   1360篇
  2007年   1189篇
  2006年   1063篇
  2005年   980篇
  2004年   967篇
  2003年   781篇
  2002年   785篇
  2001年   627篇
  2000年   633篇
  1999年   423篇
  1998年   168篇
  1997年   129篇
  1996年   120篇
  1995年   87篇
  1994年   82篇
  1993年   69篇
  1992年   158篇
  1991年   125篇
  1990年   88篇
  1989年   103篇
  1988年   71篇
  1987年   65篇
  1986年   69篇
  1985年   53篇
  1984年   47篇
  1983年   37篇
  1982年   27篇
  1981年   24篇
  1978年   28篇
  1976年   32篇
  1975年   29篇
  1973年   33篇
  1971年   23篇
  1969年   24篇
排序方式: 共有10000条查询结果,搜索用时 41 毫秒
771.
772.
773.
774.
2D nanomaterials have been found to show surface‐dominant phenomena and understanding this behavior is crucial for establishing a relationship between a material's structure and its properties. Here, the transition of molybdenum disulfide (MoS2) from a diffusion‐controlled intercalation to an emergent surface redox capacitive behavior is demonstrated. The ultrafast pseudocapacitive behavior of MoS2 becomes more prominent when the layered MoS2 is downscaled into nanometric sheets and hybridized with reduced graphene oxide (RGO). This extrinsic behavior of the 2D hybrid is promoted by the fast Faradaic charge‐transfer kinetics at the interface. The heterostructure of the 2D hybrid, as observed via high‐angle annular dark field–scanning transmission electron microscopy and Raman mapping, with a 1T MoS2 phase at the interface and a 2H phase in the bulk is associated with the synergizing capacitive performance. This 1T phase is stabilized by the interactions with the RGO. These results provide fundamental insights into the surface effects of 2D hetero‐nanosheets on emergent electrochemical properties.  相似文献   
775.
776.
777.
778.
Soft rot caused by Pectobacterium carotovorum subsp. carotovorum (Pcc) is a serious disease in Chinese cabbage (Brassica rapa L. subsp. pekinensis). To reduce the severity of soft rot symptoms in Chinese cabbage, Arabidopsis AtWRKY75 was introduced into Chinese cabbage by Agrobacterium-mediated transformation, which was previously reported to reduce susceptibility to Pcc infection in Arabidopsis. Three independent Chinese cabbage transgenic lines carrying AtWRKY75 were obtained. The growth phenotypes of AtWRKY75 overexpression (OE) lines were normal. Bacterial soft rot symptoms and Pcc growth were reduced in AtWRKY75-OE Chinese cabbage lines compared with WT plants. In contrast, overexpression of AtWRKY75 had no effect on infection with a hemibiotrophic pathogen, Xanthomonas campestris pv. campestris (Xcc) causing black rot disease. These results are consistent with those observed in the transgenic Arabidopsis. We found that AtWRKY75 activated a subset of Chinese cabbage genes related to defense against Pcc infection, such as Meri15B, BrPR4, and BrPDF1.2 (but not BrPGIP2). Moreover, overexpression of AtWRKY75 caused H2O2 production and activation of H2O2 scavenge enzyme genes, suggesting that H2O2 played a role in AtWRKY75-mediated resistance to Pcc. Together, these results demonstrated that AtWRKY75 decreased the severity of Pcc-caused bacterial soft rot and activated a subset of Pcc infection defense-related genes in Chinese cabbage similar to in Arabidopsis. It is suggested that AtWRKY75 is a candidate gene for use in crop improvement, because it results in reduced severity of disease symptoms without concurrent growth abnormalities.  相似文献   
779.
780.
Impaired autophagy in macrophages promotes inflammatory eye disease   总被引:1,自引:0,他引:1  
Autophagy is critical for maintaining cellular homeostasis. Organs such as the eye and brain are immunologically privileged. Here, we demonstrate that autophagy is essential for maintaining ocular immune privilege. Deletion of multiple autophagy genes in macrophages leads to an inflammation-mediated eye disease called uveitis that can cause blindness. Loss of autophagy activates inflammasome-mediated IL1B secretion that increases disease severity. Inhibition of caspase activity by gene deletion or pharmacological means completely reverses the disease phenotype. Of interest, experimental uveitis was also increased in a model of Crohn disease, a systemic autoimmune disease in which patients often develop uveitis, offering a potential mechanistic link between macrophage autophagy and systemic disease. These findings directly implicate the homeostatic process of autophagy in blinding eye disease and identify novel pathways for therapeutic intervention in uveitis.  相似文献   
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号