全文获取类型
收费全文 | 116篇 |
免费 | 0篇 |
专业分类
现状及发展 | 16篇 |
研究方法 | 7篇 |
综合类 | 92篇 |
自然研究 | 1篇 |
出版年
2013年 | 3篇 |
2012年 | 6篇 |
2011年 | 8篇 |
2010年 | 2篇 |
2008年 | 5篇 |
2007年 | 4篇 |
2006年 | 4篇 |
2005年 | 6篇 |
2004年 | 9篇 |
2003年 | 12篇 |
2002年 | 2篇 |
2001年 | 2篇 |
2000年 | 4篇 |
1999年 | 1篇 |
1992年 | 1篇 |
1989年 | 1篇 |
1988年 | 1篇 |
1987年 | 1篇 |
1986年 | 3篇 |
1985年 | 2篇 |
1984年 | 1篇 |
1983年 | 1篇 |
1982年 | 1篇 |
1979年 | 1篇 |
1977年 | 1篇 |
1976年 | 2篇 |
1975年 | 2篇 |
1973年 | 1篇 |
1972年 | 2篇 |
1971年 | 2篇 |
1970年 | 5篇 |
1969年 | 4篇 |
1968年 | 3篇 |
1967年 | 7篇 |
1965年 | 1篇 |
1962年 | 1篇 |
1960年 | 1篇 |
1955年 | 1篇 |
1948年 | 2篇 |
排序方式: 共有116条查询结果,搜索用时 187 毫秒
111.
112.
Population viability analysis (PVA) is widely applied in conservation biology to predict extinction risks for threatened species and to compare alternative options for their management. It can also be used as a basis for listing species as endangered under World Conservation Union criteria. However, there is considerable scepticism regarding the predictive accuracy of PVA, mainly because of a lack of validation in real systems. Here we conducted a retrospective test of PVA based on 21 long-term ecological studies--the first comprehensive and replicated evaluation of the predictive powers of PVA. Parameters were estimated from the first half of each data set and the second half was used to evaluate the performance of the model. Contrary to recent criticisms, we found that PVA predictions were surprisingly accurate. The risk of population decline closely matched observed outcomes, there was no significant bias, and population size projections did not differ significantly from reality. Furthermore, the predictions of the five PVA software packages were highly concordant. We conclude that PVA is a valid and sufficiently accurate tool for categorizing and managing endangered species. 相似文献
113.
114.
Sansone SA Rocca-Serra P Field D Maguire E Taylor C Hofmann O Fang H Neumann S Tong W Amaral-Zettler L Begley K Booth T Bougueleret L Burns G Chapman B Clark T Coleman LA Copeland J Das S de Daruvar A de Matos P Dix I Edmunds S Evelo CT Forster MJ Gaudet P Gilbert J Goble C Griffin JL Jacob D Kleinjans J Harland L Haug K Hermjakob H Ho Sui SJ Laederach A Liang S Marshall S McGrath A Merrill E Reilly D Roux M Shamu CE Shang CA Steinbeck C Trefethen A Williams-Jones B Wolstencroft K Xenarios I 《Nature genetics》2012,44(2):121-126
To make full use of research data, the bioscience community needs to adopt technologies and reward mechanisms that support interoperability and promote the growth of an open 'data commoning' culture. Here we describe the prerequisites for data commoning and present an established and growing ecosystem of solutions using the shared 'Investigation-Study-Assay' framework to support that vision. 相似文献
115.
Loveday C Turnbull C Ramsay E Hughes D Ruark E Frankum JR Bowden G Kalmyrzaev B Warren-Perry M Snape K Adlard JW Barwell J Berg J Brady AF Brewer C Brice G Chapman C Cook J Davidson R Donaldson A Douglas F Greenhalgh L Henderson A Izatt L Kumar A Lalloo F Miedzybrodzka Z Morrison PJ Paterson J Porteous M Rogers MT Shanley S Walker L;Breast Cancer Susceptibility Collaboration 《Nature genetics》2011,43(9):879-882
Recently, RAD51C mutations were identified in families with breast and ovarian cancer. This observation prompted us to investigate the role of RAD51D in cancer susceptibility. We identified eight inactivating RAD51D mutations in unrelated individuals from 911 breast-ovarian cancer families compared with one inactivating mutation identified in 1,060 controls (P = 0.01). The association found here was principally with ovarian cancer, with three mutations identified in the 59 pedigrees with three or more individuals with ovarian cancer (P = 0.0005). The relative risk of ovarian cancer for RAD51D mutation carriers was estimated to be 6.30 (95% CI 2.86-13.85, P = 4.8 × 10(-6)). By contrast, we estimated the relative risk of breast cancer to be 1.32 (95% CI 0.59-2.96, P = 0.50). These data indicate that RAD51D mutation testing may have clinical utility in individuals with ovarian cancer and their families. Moreover, we show that cells deficient in RAD51D are sensitive to treatment with a PARP inhibitor, suggesting a possible therapeutic approach for cancers arising in RAD51D mutation carriers. 相似文献
116.