全文获取类型
收费全文 | 296844篇 |
免费 | 32735篇 |
国内免费 | 330篇 |
出版年
2018年 | 2609篇 |
2016年 | 3570篇 |
2015年 | 5101篇 |
2014年 | 5699篇 |
2013年 | 8443篇 |
2012年 | 9172篇 |
2011年 | 9420篇 |
2010年 | 6273篇 |
2009年 | 5786篇 |
2008年 | 8390篇 |
2007年 | 8465篇 |
2006年 | 7976篇 |
2005年 | 7692篇 |
2004年 | 7649篇 |
2003年 | 7301篇 |
2002年 | 7080篇 |
2001年 | 12240篇 |
2000年 | 12296篇 |
1999年 | 9779篇 |
1998年 | 3617篇 |
1997年 | 3855篇 |
1996年 | 3725篇 |
1995年 | 3329篇 |
1994年 | 3310篇 |
1993年 | 3295篇 |
1992年 | 8239篇 |
1991年 | 8211篇 |
1990年 | 7879篇 |
1989年 | 7793篇 |
1988年 | 7150篇 |
1987年 | 6886篇 |
1986年 | 6252篇 |
1985年 | 6455篇 |
1984年 | 5361篇 |
1983年 | 4548篇 |
1982年 | 3541篇 |
1981年 | 3311篇 |
1980年 | 3104篇 |
1979年 | 5170篇 |
1978年 | 3996篇 |
1977年 | 3876篇 |
1976年 | 3605篇 |
1975年 | 3946篇 |
1974年 | 4334篇 |
1973年 | 4256篇 |
1972年 | 3828篇 |
1971年 | 3585篇 |
1970年 | 3211篇 |
1969年 | 3095篇 |
1968年 | 2837篇 |
排序方式: 共有10000条查询结果,搜索用时 125 毫秒
21.
22.
23.
24.
(Z)- and (E)-4-amino-2-(trifluoromethyl)-2-butenoic acid (4 and 5, respectively) were synthesized and investigated as potential mechanism-based inactivators of gamma-aminobutyric acid aminotransferase (GABA-AT) in a continuing effort to map the active site of this enzyme. The core alpha-trifluoromethyl-alpha,beta-unsaturated ester moiety was prepared via a Reformatsky/reductive elimination coupling of the key intermediates tert-butyl 2,2-dichloro-3,3,3-trifluoropropionate and N,N-bis(tert-butoxy-carbonyl)glycinal. Both 4 and 5 inhibited GABA-AT in a time-dependent manner, but displayed non-pseudo-first-order inactivation kinetics; initially, the inactivation rate increased with time. Further investigation demonstrated that the actual inactivator is generated enzymatically from 4 or 5. This inactivating species is released from the active site prior to inactivation, and as a result, 4 and 5 cannot be defined as mechanism-based inactivators. Furthermore, 4 and 5 are alternate substrates for GABA-AT, transaminated by the enzyme with Km values of 0.74 and 20.5 mM, respectively. Transamination occurs approximately 276 and 305 times per inactivation event for 4 and 5, respectively. The enzyme also catalyzes the elimination of the fluoride ion from 4 and 5. A mechanism to account for these observations is proposed. 相似文献
25.
Subsequent to observations that pulmonary responses to antigen challenge are of different magnitudes in sensitized rats that are anesthetized with different drugs, we conducted studies to test whether the alterations in responses were due to changes in airway responsiveness to cholinergic or serotonergic challenge, opioid-receptor mediated events, or changes in mast cell mediator release. Immunoglobulin E-sensitized rats anesthetized with ketamine/urethan had larger changes in lung resistance and plasma histamine after pulmonary antigen challenge compared with rats anesthetized with fentanyl-droperidol. Blockade of opioid receptors with naloxone did not affect the responses. In unsensitized rats, airway responses to aerosolized methacholine were similar for the two anesthetics, indicating unchanged smooth muscle responsiveness; however, airway responses to intravenous serotonin were enhanced by ketamine and ablated by droperidol. We conclude that ketamine- and droperidol-induced alterations of pulmonary allergic responses are due to changes in sensitivity to serotonin and in mast cell mediator release. We speculate that mast cell mediator release may be modulated by a serotonin receptor-linked mechanism. 相似文献
26.
27.
28.
Metabolic pathways involved in the oxidation of isopropanol into acetone by the intact rat 总被引:3,自引:0,他引:3
Isopropanol administered in a large (6 g/kg, orally) as well as in a lower dose (1 g/kg, I.P.) is slowly oxidized into acetone by the intact rat. Using two inhibitors, 3 amino-1,2,4-triazole and pyrazole, investigations on the hepatic enzymatic system involved in the oxidation of isopropanol show that catalase does not play an important part in this pathway, contrary to alcohol dehydrogenase which is the major enzyme responsible for this oxidation. Although isopropanol oxidation is mainly catalysed in the liver through alcohol dehydrogenase, no alteration of the hepatic extramitochondrial redox state occurs after the administration of a large as well as of a lower dose of isopropanol. From these experiments it may be concluded that alterations of the liver NAD+/NADH ratio, which seem to play an important part in the ethanol induced fatty liver, are not involved in the isopropanol induced one. 相似文献
29.
30.
Ca2+ channel antagonist actions in bladder smooth muscle: comparative pharmacologic and [3H]nitrendipine binding studies 总被引:2,自引:0,他引:2
F B Yousif G T Bolger A Ruzycky D J Triggle 《Canadian journal of physiology and pharmacology》1985,63(5):453-462
The actions of a series of 15 Ca2+ channel antagonists including D-600, nifedipine, and diltiazem were examined against K+ depolarization and muscarinic receptor induced responses in guinea pig bladder smooth muscle. Responses of bladder are very dependent upon extracellular Ca2+ and sensitive to the Ca2+ channel antagonists, the tonic component more than the phasic component of response. Regardless of stimulant, K+ or methylfurmethide (MF), or component of response, the same rank order of antagonist activities is expressed, suggestive of a single structure-activity relationship and the existence of a single category of binding site which may, however, exist in several affinity states. High affinity binding of [3H]nitrendipine (KD = 1.1 X 10(-10) M) occurs in bladder membranes, and similar high affinity binding was found in microsomal preparations from other smooth muscles including guinea pig and rat lung, rat vas deferens, uterus, and stomach. [3H]nitrendipine binding in the bladder was sensitive to displacement by other 1,4-dihydropyridines, paralleling their pharmacologic activities and showing excellent agreement with binding data previously obtained for guinea pig ileal smooth muscle. Comparison of pharmacologic data for inhibition of K+- and MF-induced responses by a common series of Ca2+ channel antagonists in bladder and ileum revealed excellent correlations. Neither pharmacologic nor binding studies suggest significant differences in Ca2+ channel antagonist properties in smooth muscle from bladder and intestine. 相似文献