全文获取类型
收费全文 | 1156篇 |
免费 | 211篇 |
专业分类
1367篇 |
出版年
2021年 | 10篇 |
2019年 | 12篇 |
2017年 | 9篇 |
2016年 | 15篇 |
2015年 | 23篇 |
2014年 | 30篇 |
2013年 | 34篇 |
2012年 | 38篇 |
2011年 | 53篇 |
2010年 | 40篇 |
2009年 | 26篇 |
2008年 | 52篇 |
2007年 | 48篇 |
2006年 | 37篇 |
2005年 | 46篇 |
2004年 | 46篇 |
2003年 | 40篇 |
2002年 | 40篇 |
2001年 | 43篇 |
2000年 | 37篇 |
1999年 | 42篇 |
1998年 | 18篇 |
1997年 | 12篇 |
1996年 | 21篇 |
1995年 | 16篇 |
1994年 | 16篇 |
1993年 | 13篇 |
1992年 | 34篇 |
1991年 | 20篇 |
1990年 | 34篇 |
1989年 | 33篇 |
1988年 | 26篇 |
1987年 | 31篇 |
1986年 | 14篇 |
1985年 | 20篇 |
1984年 | 29篇 |
1983年 | 17篇 |
1982年 | 13篇 |
1981年 | 13篇 |
1980年 | 13篇 |
1979年 | 12篇 |
1978年 | 14篇 |
1977年 | 15篇 |
1976年 | 17篇 |
1975年 | 17篇 |
1974年 | 14篇 |
1973年 | 14篇 |
1972年 | 9篇 |
1971年 | 8篇 |
1942年 | 10篇 |
排序方式: 共有1367条查询结果,搜索用时 0 毫秒
111.
Alpha-conotoxins ImI and ImII. Similar alpha 7 nicotinic receptor antagonists act at different sites
A novel conotoxin, alpha-conotoxin ImII (alpha-CTx ImII), identified from Conus imperialis venom ducts, was chemically synthesized. A previously characterized C. imperialis conotoxin, alpha-conotoxin ImI (alpha-CTx ImI), is closely related; 9 of 12 amino acids are identical. Both alpha-CTx ImII and alpha-CTx ImI functionally inhibit heterologously expressed rat alpha7 nAChRs with similar IC(50) values. Furthermore, the biological activities of intracranially applied alpha-CTx ImI and alpha-CTx ImII are similar over the same dosage range, and are consistent with alpha7 nAChR inhibition. However, unlike alpha-CTx ImI, alpha-CTx ImII was not able to block the binding of alpha-bungarotoxin to alpha7 nAChRs. alpha-Conotoxin ImI and alpha-bungarotoxin-binding sites have been well characterized as overlapping and located at the cleft between adjacent nAChR subunits. Because alpha-CTx ImI and alpha-CTx ImII share extensive sequence homology, the inability of alpha-CTx ImII to compete with alpha-BgTx is surprising. Furthermore, functional studies in oocytes indicate that there is no overlap between functional binding sites of alpha-CTx ImI and alpha-CTx ImII. Like alpha-CTx ImI, the block by alpha-CTx ImII is voltage-independent. Thus, alpha-CTx ImII represents a probe for a novel antagonist binding site, or microsite, on the alpha7 nAChR. 相似文献
112.
113.
The xylanase, BadX, from the alkalophilic Bacillus agaradhaerens was cloned, expressed and studied in comparison to a related family 11 xylanase, BcX, from B. circulans. Despite the alkaline versus neutral conditions under which these bacteria grow, BadX and BcX both exhibit optimal activity near pH 5.6 using the substrate o-nitrophenyl beta-xylobioside. Analysis of the bell-shaped activity profile of BadX yielded apparent pK(a) values of 4.2 and 7.1, assignable to its nucleophile Glu94 and general acid Glu184, respectively. In addition to having an approximately 10-fold higher k(cat)/K(m) value with this substrate at pH 6 and 40 degrees C, BadX has significantly higher thermal stability than BcX under neutral and alkaline conditions. This enhanced stability, rather than a shift in its pH-optimum, may allow BadX to hydrolyze xylan under conditions of elevated temperature and pH. 相似文献
114.
115.
116.
Pospisilik JA Hinke SA Pederson RA Hoffmann T Rosche F Schlenzig D Glund K Heiser U McIntosh CH Demuth H 《Regulatory peptides》2001,96(3):133-141
Glucagon is a 29-amino acid polypeptide released from pancreatic islet alpha-cells that acts to maintain euglycemia by stimulating hepatic glycogenolysis and gluconeogenesis. Despite its importance, there remains controversy about the mechanisms responsible for glucagon clearance in the body. In the current study, enzymatic metabolism of glucagon was assessed using sensitive mass spectrometric techniques to identify the molecular products. Incubation of glucagon with purified porcine dipeptidyl peptidase IV (DP IV) yielded sequential production of glucagon(3-29) and glucagon(5-29). In human serum, degradation to glucagon(3-29) was rapidly followed by N-terminal cyclization of glucagon, preventing further DP IV-mediated hydrolysis. Bioassay of glucagon, following incubation with purified DP IV or normal rat serum demonstrated a significant loss of hyperglycemic activity, while a similar incubation in DP IV-deficient rat serum did not show any loss of glucagon bioactivity. Degradation, monitored by mass spectrometry and bioassay, was blocked by the specific DP IV inhibitor, isoleucyl thiazolidine. These results identify DP IV as a primary enzyme involved in the degradation and inactivation of glucagon. These findings have important implications for the determination of glucagon levels in human plasma. 相似文献
117.
118.
119.
120.