全文获取类型
收费全文 | 116篇 |
免费 | 12篇 |
出版年
2022年 | 1篇 |
2020年 | 3篇 |
2019年 | 1篇 |
2018年 | 3篇 |
2016年 | 1篇 |
2015年 | 5篇 |
2014年 | 9篇 |
2013年 | 5篇 |
2012年 | 3篇 |
2011年 | 3篇 |
2010年 | 3篇 |
2009年 | 3篇 |
2008年 | 5篇 |
2007年 | 2篇 |
2006年 | 2篇 |
2005年 | 3篇 |
2004年 | 3篇 |
2003年 | 2篇 |
2002年 | 3篇 |
2001年 | 2篇 |
2000年 | 1篇 |
1999年 | 3篇 |
1998年 | 3篇 |
1997年 | 3篇 |
1996年 | 1篇 |
1995年 | 1篇 |
1994年 | 2篇 |
1992年 | 3篇 |
1991年 | 1篇 |
1990年 | 5篇 |
1989年 | 3篇 |
1988年 | 4篇 |
1987年 | 5篇 |
1985年 | 3篇 |
1984年 | 2篇 |
1983年 | 1篇 |
1982年 | 1篇 |
1981年 | 1篇 |
1979年 | 1篇 |
1977年 | 3篇 |
1976年 | 2篇 |
1974年 | 1篇 |
1972年 | 2篇 |
1971年 | 2篇 |
1965年 | 1篇 |
1964年 | 1篇 |
1960年 | 2篇 |
1959年 | 3篇 |
1958年 | 2篇 |
1957年 | 3篇 |
排序方式: 共有128条查询结果,搜索用时 15 毫秒
71.
Ager BP 《Trends in ecology & evolution》1988,3(4):S42-S44
The environment does not recognize national boundaries. Nor, increasingly, does trade. There is, therefore, a need to harmonize the regulation of the planned release of organisms containing recombinant DNA. This is particularly important for the geographically and economically interdependent countries in Europe. The various nations within the European Community have responded differently to proposals for planned release. An important step towards harmonization has been made with the OECD report on recombinant DNA. Yet there is still scope for a Community-wide framework of regulation. 相似文献
72.
A total X-ray dose of 50 Gy was applied to the nematode Panagrellus redivivus using dose-rates ranging from 0.23 Gy/min to 10.49 Gy/min, and the frequency of lethal X-chromosomes was determined. This frequency ranged from approximately 1.6% at the lower dose-rate to 4.3% at the highest dose-rate, indicating a dose-rate dependency of mutation frequency in the spermatogonia and oogonia of this organism. 相似文献
73.
Christine Roxanne Hung Linda Ager‐Wick Ellingsen Guillaume Majeau‐Bettez 《Journal of Industrial Ecology》2020,24(1):26-37
While life cycle assessment (LCA) is a tool often used to evaluate the environmental impacts of products and technologies, the amount of data required to perform such studies make the evaluation of emerging technologies using the conventional LCA approach challenging. The development paradox is such that the inputs from a comprehensive environmental assessment has the greatest effect early in the development phase, and yet the data required to perform such an assessment are generally lacking until it is too late. Previous attempts to formalize strategies for performing streamlined or screening LCAs were made in the late 1990s and early 2000s, mostly to rapidly compare the environmental performance of product design candidates. These strategies lack the transparency and consistency required for the environmental screening of large numbers of early‐development candidates, for which data are even sparser. We propose the Lifecycle Screening of Emerging Technologies method (LiSET). LiSET is an adaptable screening‐to‐LCA method that uses the available data to systematically and transparently evaluate the environmental performance of technologies at low readiness levels. Iterations follow technological development and allow a progression to a full LCA if desired. In early iterations, LiSET presents results in a matrix structure combined with a “traffic light” color grading system. This format inherently communicates the high uncertainty of analysis at this stage and presents numerous environmental aspects assessed. LiSET takes advantage of a decomposition analysis and data not traditionally used in LCAs to gain insight to the life cycle impacts and ensure that the most environmentally sustainable technologies are adopted. 相似文献
74.
Rapkins RW Hore T Smithwick M Ager E Pask AJ Renfree MB Kohn M Hameister H Nicholls RD Deakin JE Graves JA 《PLoS genetics》2006,2(10):e182
Genomic imprinting, representing parent-specific expression of alleles at a locus, raises many questions about how—and especially why—epigenetic silencing of mammalian genes evolved. We present the first in-depth study of how a human imprinted domain evolved, analyzing a domain containing several imprinted genes that are involved in human disease. Using comparisons of orthologous genes in humans, marsupials, and the platypus, we discovered that the Prader-Willi/Angelman syndrome region on human Chromosome 15q was assembled only recently (105–180 million years ago). This imprinted domain arose after a region bearing UBE3A (Angelman syndrome) fused with an unlinked region bearing SNRPN (Prader-Willi syndrome), which had duplicated from the non-imprinted SNRPB/B′. This region independently acquired several retroposed gene copies and arrays of small nucleolar RNAs from different parts of the genome. In their original configurations, SNRPN and UBE3A are expressed from both alleles, implying that acquisition of imprinting occurred after their rearrangement and required the evolution of a control locus. Thus, the evolution of imprinting in viviparous mammals is ongoing. 相似文献
75.
76.
77.
78.
79.
Y Cheng X Ren A SP Gowda Y Shan L Zhang Y-S Yuan R Patel H Wu K Huber-Keener J W Yang D Liu T E Spratt J-M Yang 《Cell death & disease》2013,4(7):e731
Sirtuin 3 (Sirt3), a major mitochondrial NAD+-dependent deacetylase, targets various mitochondrial proteins for lysine deacetylation and regulates important cellular functions such as energy metabolism, aging, and stress response. In this study, we identified the human 8-oxoguanine-DNA glycosylase 1 (OGG1), a DNA repair enzyme that excises 7,8-dihydro-8-oxoguanine (8-oxoG) from damaged genome, as a new target protein for Sirt3. We found that Sirt3 physically associated with OGG1 and deacetylated this DNA glycosylase and that deacetylation by Sirt3 prevented the degradation of the OGG1 protein and controlled its incision activity. We further showed that regulation of the acetylation and turnover of OGG1 by Sirt3 played a critical role in repairing mitochondrial DNA (mtDNA) damage, protecting mitochondrial integrity, and preventing apoptotic cell death under oxidative stress. We observed that following ionizing radiation, human tumor cells with silencing of Sirt3 expression exhibited deteriorated oxidative damage of mtDNA, as measured by the accumulation of 8-oxoG and 4977 common deletion, and showed more severe mitochondrial dysfunction and underwent greater apoptosis in comparison with the cells without silencing of Sirt3 expression. The results reported here not only reveal a new function and mechanism for Sirt3 in defending the mitochondrial genome against oxidative damage and protecting from the genotoxic stress-induced apoptotic cell death but also provide evidence supporting a new mtDNA repair pathway. 相似文献
80.
Nick J Willett Tanushree Thote Angela SP Lin Shamus Moran Yazdan Raji Sanjay Sridaran Hazel Y Stevens Robert E Guldberg 《Arthritis research & therapy》2014,16(1):R47