全文获取类型
收费全文 | 763篇 |
免费 | 61篇 |
专业分类
824篇 |
出版年
2023年 | 3篇 |
2022年 | 9篇 |
2021年 | 7篇 |
2020年 | 18篇 |
2019年 | 16篇 |
2018年 | 17篇 |
2017年 | 7篇 |
2016年 | 21篇 |
2015年 | 44篇 |
2014年 | 43篇 |
2013年 | 74篇 |
2012年 | 55篇 |
2011年 | 55篇 |
2010年 | 48篇 |
2009年 | 43篇 |
2008年 | 43篇 |
2007年 | 39篇 |
2006年 | 30篇 |
2005年 | 26篇 |
2004年 | 29篇 |
2003年 | 23篇 |
2002年 | 21篇 |
2001年 | 10篇 |
2000年 | 5篇 |
1999年 | 8篇 |
1998年 | 14篇 |
1997年 | 12篇 |
1996年 | 8篇 |
1995年 | 9篇 |
1994年 | 5篇 |
1993年 | 9篇 |
1992年 | 2篇 |
1991年 | 4篇 |
1990年 | 2篇 |
1989年 | 3篇 |
1988年 | 7篇 |
1985年 | 4篇 |
1984年 | 4篇 |
1983年 | 3篇 |
1982年 | 16篇 |
1981年 | 3篇 |
1979年 | 2篇 |
1978年 | 2篇 |
1977年 | 5篇 |
1976年 | 4篇 |
1975年 | 3篇 |
1972年 | 1篇 |
1971年 | 2篇 |
1963年 | 2篇 |
1926年 | 1篇 |
排序方式: 共有824条查询结果,搜索用时 0 毫秒
821.
Marjan De Mey Gaspard J. Lequeux Jo Maertens Cassandra I. De Muynck Wim K. Soetaert Erick J. Vandamme 《Biologicals》2008,36(3):198-202
Many different extraction and analysis methods exist to determine the protein fraction of microbial cells. For metabolic engineering purposes it is important to have precise and accurate measurements. Therefore six different protein extraction protocols and seven protein quantification methods were tested and compared. Comparison was based on the reliability of the methods and boxplots of the normalized residuals. Some extraction techniques (SDS/chloroform and toluene) should never be used: the measurements are neither precise nor accurate. Bugbuster extraction combined with UV280 quantification gives the best results, followed by the combinations Sonication-UV280 and EasyLyse-UV280. However, if one does not want to use the quantification method UV280, one can opt to use Bugbuster, EasyLyse or sonication extraction combined with any quantification method with exception of the EasyLyse-BCA_P and Sonication-BCA_P combinations. 相似文献
822.
823.
Mouse models have been widely used to elucidate the pathogenic mechanisms of human diseases. The advantages of using these models include the ability to study different stages of the disease with particular respect to specific target organs, to focus on the role of specific pathogenic factors and to investigate the effect of possible therapeutic interventions. Sjögren’s syndrome (SS) is a systemic autoimmune disease, characterised by lymphocytic infiltrates in the salivary and lacrimal glands. To date, effective therapy is not available and treatment has been mainly symptomatic. Ongoing studies in murine models are aimed at developing more effective and targeted therapies in SS. The heterogeneity of SS will most probably benefit from optimising therapies, tailored to specific subgroups of the disease. In this review, we provide our perspective on the importance of subdividing SS patients according to their interferon signature, and recommend choosing appropriate mouse models for interferon-positive and interferon-negative SS subtypes. Murine models better resembling human-disease phenotypes will be essential in this endeavour. 相似文献
824.
Marjan Huizing Raymond E. Boissy William A. Gahl 《Pigment cell & melanoma research》2002,15(6):405-419
The disorders known as Hermansky–Pudlak syndrome (HPS) are a group of genetic diseases resulting from abnormal formation of intracellular vesicles. In HPS, dysfunction of melanosomes results in oculocutaneous albinism, and absence of platelet dense bodies causes a bleeding diathesis. In addition, some HPS patients suffer granulomatous colitis or fatal pulmonary fibrosis, perhaps due to mistrafficking of a subset of lysosomes. The impaired function of specific organelles indicates that the causative genes encode proteins operative in the formation of certain vesicles. Four such genes, HPS1, ADTB3A, HPS3, and HPS4, are associated with the four known subtypes of HPS, i.e. HPS‐1, HPS‐2, HPS‐3, and HPS‐4. ADTB3A codes for the β3A subunit of adaptor complex‐3, known to assist in vesicle formation from the trans‐Golgi network or late endosome. However, the functions of the HPS1, HPS3, and HPS4 gene products remain unknown. These three genes arose with the evolution of mammals and have no homologs in yeast, reflecting their specialized function. In contrast, all four known HPS‐causing genes have homologs in mice, a species with 14 different models of HPS, i.e. hypopigmentation and a platelet storage pool deficiency. Pursuit of the mechanism of mammalian vesicle formation and trafficking, impaired in HPS, relies upon investigation of these mouse models as well as studies of protein complexes involved in yeast vacuole formation. 相似文献