全文获取类型
收费全文 | 131篇 |
免费 | 45篇 |
出版年
2024年 | 1篇 |
2023年 | 1篇 |
2022年 | 4篇 |
2021年 | 7篇 |
2020年 | 2篇 |
2019年 | 1篇 |
2018年 | 2篇 |
2017年 | 2篇 |
2016年 | 5篇 |
2015年 | 7篇 |
2014年 | 7篇 |
2013年 | 4篇 |
2012年 | 15篇 |
2011年 | 10篇 |
2010年 | 9篇 |
2009年 | 4篇 |
2008年 | 10篇 |
2007年 | 3篇 |
2006年 | 2篇 |
2005年 | 2篇 |
2004年 | 2篇 |
2003年 | 3篇 |
2002年 | 2篇 |
2001年 | 1篇 |
2000年 | 1篇 |
1999年 | 1篇 |
1998年 | 3篇 |
1997年 | 1篇 |
1995年 | 1篇 |
1994年 | 2篇 |
1993年 | 1篇 |
1992年 | 1篇 |
1991年 | 1篇 |
1989年 | 3篇 |
1988年 | 37篇 |
1987年 | 11篇 |
1986年 | 2篇 |
1985年 | 2篇 |
1982年 | 1篇 |
1979年 | 1篇 |
1964年 | 1篇 |
排序方式: 共有176条查询结果,搜索用时 15 毫秒
81.
82.
83.
Effects of biochar amendment on root traits and contaminant availability of maize plants in a copper and arsenic impacted soil 总被引:1,自引:0,他引:1
Aoife Brennan Eduardo Moreno Jiménez Markus Puschenreiter José Antonio Alburquerque Christine Switzer 《Plant and Soil》2014,379(1-2):351-360
Background and aims
Biochar has been proposed as a tool to enhance phytostabilisation of contaminated soils but little data are available to illustrate the direct effect on roots in contaminated soils. This work aimed to investigate specific root traits and to assess the effect of biochar amendment on contaminant availability.Methods
Amendment with two different types of biochar, pine woodchip and olive tree pruning, was assessed in a rhizobox experiment with maize planted in a soil contaminated with significant levels of copper and arsenic.Results
Amendment was found to significantly improve root traits compared to the control soil, particularly root mass density and root length density. Copper uptake to plants and ammonium sulphate extractable copper was significantly less in the biochar amended soils. Arsenic uptake and extractability varied with type of biochar used but was not considered to be the limiting factor affecting root and shoot development.Conclusions
Root establishment in contaminated soils can be enhanced by biochar amendment but choice of biochar is key to maximising soil improvement and controlling contaminant availability. 相似文献84.
85.
86.
Noonan J Tanveer R Klompas A Gowran A McKiernan J Campbell VA 《The Journal of biological chemistry》2010,285(49):38543-38554
Neuronal cell loss underlies the pathological decline in cognition and memory associated with Alzheimer disease (AD). Recently, targeting the endocannabinoid system in AD has emerged as a promising new approach to treatment. Studies have identified neuroprotective roles for endocannabinoids against key pathological events in the AD brain, including cell death by apoptosis. Elucidation of the apoptotic pathway evoked by β-amyloid (Aβ) is thus important for the development of therapeutic strategies that can thwart Aβ toxicity and preserve cell viability. We have previously reported that lysosomal membrane permeabilization plays a distinct role in the apoptotic pathway initiated by Aβ. In the present study, we provide evidence that the endocannabinoid system can stabilize lysosomes against Aβ-induced permeabilization and in turn sustain cell survival. We report that endocannabinoids stabilize lysosomes by preventing the Aβ-induced up-regulation of the tumor suppressor protein, p53, and its interaction with the lysosomal membrane. We also provide evidence that intracellular cannabinoid type 1 receptors play a role in stabilizing lysosomes against Aβ toxicity and thus highlight the functionality of these receptors. Given the deleterious effect of lysosomal membrane permeabilization on cell viability, stabilization of lysosomes with endocannabinoids may represent a novel mechanism by which these lipid modulators confer neuroprotection. 相似文献
87.
Doherty Aoife Lopes Inês Ford Christopher T. Monaco Gianni Guest Patrick de Magalhães João Pedro 《Mammalian genome》2020,31(7-8):215-227
Mammalian Genome - Selective breeding of the domestic dog (Canis lupus familiaris) rigidly retains desirable features, and could inadvertently fix disease-causing variants within a breed. We... 相似文献
88.
89.
Martel MA Ryan TJ Bell KF Fowler JH McMahon A Al-Mubarak B Komiyama NH Horsburgh K Kind PC Grant SG Wyllie DJ Hardingham GE 《Neuron》2012,74(3):543-556
It is currently unclear whether the GluN2 subtype influences NMDA receptor (NMDAR) excitotoxicity. We report that the toxicity of NMDAR-mediated Ca(2+) influx is differentially controlled by the cytoplasmic C-terminal domains of GluN2B (CTD(2B)) and GluN2A (CTD(2A)). Studying the effects of acute expression of GluN2A/2B-based chimeric subunits with reciprocal exchanges of their CTDs revealed that CTD(2B) enhances NMDAR toxicity, compared to CTD(2A). Furthermore, the vulnerability of forebrain neurons in?vitro and in?vivo to NMDAR-dependent Ca(2+) influx is lowered by replacing the CTD of GluN2B with that of GluN2A by targeted exon exchange in a mouse knockin model. Mechanistically, CTD(2B) exhibits stronger physical/functional coupling to the PSD-95-nNOS pathway, which suppresses protective CREB activation. Dependence of NMDAR excitotoxicity on the GluN2 CTD subtype can be overcome by inducing high levels of NMDAR activity. Thus, the identity (2A versus 2B) of the GluN2 CTD controls the toxicity dose-response to episodes of NMDAR activity. 相似文献
90.