全文获取类型
收费全文 | 220篇 |
免费 | 28篇 |
专业分类
248篇 |
出版年
2022年 | 3篇 |
2021年 | 6篇 |
2019年 | 3篇 |
2018年 | 2篇 |
2017年 | 3篇 |
2016年 | 11篇 |
2015年 | 12篇 |
2014年 | 8篇 |
2013年 | 14篇 |
2012年 | 6篇 |
2011年 | 10篇 |
2010年 | 7篇 |
2009年 | 10篇 |
2008年 | 5篇 |
2007年 | 7篇 |
2006年 | 5篇 |
2005年 | 2篇 |
2004年 | 8篇 |
2003年 | 6篇 |
2002年 | 6篇 |
2001年 | 4篇 |
2000年 | 3篇 |
1999年 | 6篇 |
1998年 | 8篇 |
1997年 | 2篇 |
1996年 | 5篇 |
1995年 | 4篇 |
1994年 | 3篇 |
1993年 | 3篇 |
1992年 | 3篇 |
1991年 | 6篇 |
1990年 | 6篇 |
1989年 | 4篇 |
1988年 | 3篇 |
1987年 | 7篇 |
1986年 | 6篇 |
1985年 | 5篇 |
1983年 | 2篇 |
1982年 | 2篇 |
1981年 | 3篇 |
1980年 | 2篇 |
1979年 | 2篇 |
1978年 | 4篇 |
1977年 | 6篇 |
1976年 | 2篇 |
1975年 | 2篇 |
1974年 | 2篇 |
1973年 | 2篇 |
1971年 | 3篇 |
1955年 | 1篇 |
排序方式: 共有248条查询结果,搜索用时 15 毫秒
41.
42.
Immunoprecipitation of lipid transfer protein activity by an antibody against human plasma lipid transfer protein-I 总被引:2,自引:0,他引:2
Two lipid transfer proteins, designated lipid transfer protein-I (Mr 69 000) and lipid transfer protein-II (Mr 55 000), each of which facilitates the transfer of radiolabelled cholesteryl ester, triacylglycerol and phosphatidylcholine between plasma lipoproteins, were purified from human plasma. Immunoglobulin G was prepared from goat antiserum to human lipid transfer protein-I (i.e., anti-human LTP-I IgG). The progressive addition of anti-human LTP-I IgG to buffered solutions containing either a highly purified mixture of human lipid transfer protein-I and lipid transfer protein-II, or highly purified rabbit lipid transfer protein (Abbey, M., Calvert, G.D. and Barter, P.J. (1984) Biochim. Biophys. Acta 793, 471-480) resulted in specific immunoprecipitation and the removal of increasing amounts, up to 100%, of cholesteryl ester, triacylglycerol and phosphatidylcholine transfer activities. However, similar precipitation studies on human and rabbit lipoprotein-free plasma resulted in the progressive removal of all cholesteryl ester and triacylglycerol transfer activities but only 30% (human) or 20% (rabbit) of phosphatidylcholine transfer activity. In all cases more anti-human LTP-I IgG was required to precipitate rabbit lipid transfer activity than human lipid transfer activity. These results suggest that lipid transfer protein-I and lipid transfer protein-II have antigenic sites in common, allowing precipitation of both proteins by specific antibody to lipid transfer protein-I. Most plasma phosphatidylcholine transfer activity is mediated by a protein (or proteins) other than lipid transfer protein-I and lipid transfer protein-II. In lipoprotein-free plasma all cholesteryl ester and triacylglycerol transfer activity, and some phosphatidylcholine transfer activity, is mediated by lipid transfer protein-I (or lipid transfer protein-I and an antigenically similar protein, lipid transfer protein-II. 相似文献
43.
Two distinct conformational states define the interaction of human RAD51‐ATP with single‐stranded DNA 下载免费PDF全文
Andrea Candelli Edwige B Garcin Mauro Modesti Luca Pellegrini Gijs JL Wuite Erwin JG Peterman 《The EMBO journal》2018,37(7)
An essential mechanism for repairing DNA double‐strand breaks is homologous recombination (HR). One of its core catalysts is human RAD51 (hRAD51), which assembles as a helical nucleoprotein filament on single‐stranded DNA, promoting DNA‐strand exchange. Here, we study the interaction of hRAD51 with single‐stranded DNA using a single‐molecule approach. We show that ATP‐bound hRAD51 filaments can exist in two different states with different contour lengths and with a free‐energy difference of ~4 kBT per hRAD51 monomer. Upon ATP hydrolysis, the filaments convert into a disassembly‐competent ADP‐bound configuration. In agreement with the single‐molecule analysis, we demonstrate the presence of two distinct protomer interfaces in the crystal structure of a hRAD51‐ATP filament, providing a structural basis for the two conformational states of the filament. Together, our findings provide evidence that hRAD51‐ATP filaments can exist in two interconvertible conformational states, which might be functionally relevant for DNA homology recognition and strand exchange. 相似文献
44.
Caitlin Kozel Brytteny Thompson Samantha Hustak Chelsea Moore Akio Nakashima Chingakham Ranjit Singh Megan Reid Christian Cox Evangelos Papadopoulos Rafael E. Luna Abbey Anderson Hideaki Tagami Hiroyuki Hiraishi Emily Archer Slone Ken-ichi Yoshino Masayo Asano Sarah Gillaspie Jerome Nietfeld Jean-Pierre Perchellet Stefan Rothenburg Hisao Masai Gerhard Wagner Alexander Beeser Ushio Kikkawa Sherry D. Fleming Katsura Asano 《Nucleic acids research》2016,44(18):8704-8713
45.
C Zinner M Krueger JL Reed M Kohl-Bareis H-C Holmberg B Sperlich 《Biology of sport / Institute of Sport》2016,33(1):71-76
In this study, we tested the hypothesis that breathing hyperoxic air (FinO2 = 0.40) while exercising in a hot environment exerts negative effects on the total tissue level of haemoglobin concentration (tHb); core (Tcore) and skin (Tskin) temperatures; muscle activity; heart rate; blood concentration of lactate; pH; partial pressure of oxygen (PaO2) and carbon dioxide; arterial oxygen saturation (SaO2); and perceptual responses. Ten well-trained male athletes cycled at submaximal intensity at 21°C or 33°C in randomized order: first for 20 min while breathing normal air (FinO2 = 0.21) and then 10 min with FinO2 = 0.40 (HOX). At both temperatures, SaO2 and PaO2, but not tHb, were increased by HOX. Tskin and perception of exertion and thermal discomfort were higher at 33°C than 21°C (p < 0.01), but independent of FinO2. Tcore and muscle activity were the same under all conditions (p > 0.07). Blood lactate and heart rate were higher at 33°C than 21°C. In conclusion, during 30 min of submaximal cycling at 21°C or 33°C, Tcore, Tskin and Tbody, tHb, muscle activity and ratings of perceived exertion and thermal discomfort were the same under normoxic and hyperoxic conditions. Accordingly, breathing hyperoxic air (FinO2 = 0.40) did not affect thermoregulation under these conditions. 相似文献
46.
47.
48.
49.
50.
A modular treatment of molecular traffic through the active site of cholinesterase 总被引:1,自引:0,他引:1 下载免费PDF全文
We present a model for the molecular traffic of ligands, substrates, and products through the active site of cholinesterases (ChEs). First, we describe a common treatment of the diffusion to a buried active site of cationic and neutral species. We then explain the specificity of ChEs for cationic ligands and substrates by introducing two additional components to this common treatment. The first module is a surface trap for cationic species at the entrance to the active-site gorge that operates through local, short-range electrostatic interactions and is independent of ionic strength. The second module is an ionic-strength-dependent steering mechanism generated by long-range electrostatic interactions arising from the overall distribution of charges in ChEs. Our calculations show that diffusion of charged ligands relative to neutral isosteric analogs is enhanced approximately 10-fold by the surface trap, while electrostatic steering contributes only a 1.5- to 2-fold rate enhancement at physiological salt concentration. We model clearance of cationic products from the active-site gorge as analogous to the escape of a particle from a one-dimensional well in the presence of a linear electrostatic potential. We evaluate the potential inside the gorge and provide evidence that while contributing to the steering of cationic species toward the active site, it does not appreciably retard their clearance. This optimal fine-tuning of global and local electrostatic interactions endows ChEs with maximum catalytic efficiency and specificity for a positively charged substrate, while at the same time not hindering clearance of the positively charged products. 相似文献