全文获取类型
收费全文 | 180篇 |
免费 | 11篇 |
国内免费 | 7篇 |
专业分类
儿科学 | 4篇 |
基础医学 | 7篇 |
口腔科学 | 1篇 |
临床医学 | 17篇 |
内科学 | 8篇 |
皮肤病学 | 1篇 |
神经病学 | 8篇 |
特种医学 | 2篇 |
外科学 | 11篇 |
综合类 | 32篇 |
预防医学 | 2篇 |
眼科学 | 2篇 |
药学 | 68篇 |
中国医学 | 35篇 |
出版年
2023年 | 1篇 |
2022年 | 4篇 |
2021年 | 4篇 |
2020年 | 6篇 |
2019年 | 3篇 |
2018年 | 4篇 |
2017年 | 6篇 |
2016年 | 5篇 |
2015年 | 2篇 |
2014年 | 13篇 |
2013年 | 16篇 |
2012年 | 14篇 |
2011年 | 18篇 |
2010年 | 14篇 |
2009年 | 9篇 |
2008年 | 13篇 |
2007年 | 9篇 |
2006年 | 5篇 |
2005年 | 6篇 |
2004年 | 2篇 |
2003年 | 2篇 |
2002年 | 4篇 |
2001年 | 4篇 |
2000年 | 3篇 |
1999年 | 3篇 |
1997年 | 3篇 |
1996年 | 2篇 |
1994年 | 1篇 |
1993年 | 1篇 |
1992年 | 2篇 |
1990年 | 3篇 |
1989年 | 1篇 |
1987年 | 1篇 |
1985年 | 1篇 |
1984年 | 3篇 |
1981年 | 1篇 |
1980年 | 1篇 |
1979年 | 1篇 |
1978年 | 1篇 |
1977年 | 1篇 |
1975年 | 2篇 |
1972年 | 1篇 |
1970年 | 1篇 |
1968年 | 1篇 |
排序方式: 共有198条查询结果,搜索用时 15 毫秒
11.
12.
目的 通过体外培养体法考察镇静催眠药(安定、咪达唑仑和苯巴比妥)对阿司匹林酯酶活性的影响。方法 采用实验室建立的阿司匹林酯酶体外代谢系统,用高效液相色谱直接进样法测定培养体系中阿司匹林(ASA)和水杨酸(SA)的浓度,以SA/(ASA+SA)比值反应阿司匹林酯酶的活性。通过在培养体系中加入或不加安定、咪达唑仑和苯巴比妥时阿司匹林酯酶活性的变化,分析上述镇静催眠药对阿司匹林酯酶活性的影响。结果 安定、咪达唑仑、苯巴比妥对阿司匹林酯酶活性的影响分别为-10.71%(P>0.05)、-27.94%(P<0.05)和8.83%(P<0.05),咪达唑仑对阿司匹林酯酶的活性有一定的抑制作用,苯巴比妥对阿司匹林酯酶的活性有一定的诱导作用。结论 咪达唑仑、苯巴比妥与阿司匹林合用时应注意药物间的相互作用。 相似文献
13.
Apoptosis occurs physiologically in the mammalian brain during the period of the growth spurt, which in human starts in the 3rd trimester of gestation and ends by the third year of life. Environmental factors can interact with programmed cell death mechanisms to increase the number of neurons undergoing apoptosis and thus produce neuropathological sequelae in the brain. In a series of studies it could be shown that classes of drugs which block N-methyl-d-aspartate (NMDA) glutamate receptors, promote γ-aminobutyric-acid (GABAA) receptor activation or block voltage gated sodium channels, when administered to immature rodents during the period of the brain growth spurt, trigger widespread apoptotic neurodegeneration throughout the developing brain. Studies have also shown that short exposures to non-physiologic oxygen levels can trigger apoptotic neurodegeneration in the brains of infant rodents. Pathomechanisms involved in the proapoptotic action of sedative and anticonvulsant drugs and oxygen include decreased expression of neurotrophins, inactivation of survival signaling proteins, activation of inflammatory cytokines as well as oxidative stress. These findings raise concerns pertaining to the treatment of infants and young children with sedative and anticonvulsant drugs and premature infants with oxygen. The experimental findings imply that new approaches should be developed for patients within these vulnerable age groups. 相似文献
14.
Celso A. Rodrigues de Almeida CostaDaniele Oliveira Kohn Valéria Martins de LimaAndré Costa Gargano Jorge Camilo FlórioMirtes Costa 《Journal of ethnopharmacology》2011,137(1):828-836
Ethnopharmacological relevance
The essential oil (EO) from Cymbopogon citratus (DC) Stapf is reported to have a wide range of biological activities and is widely used in traditional medicine as an infusion or decoction. However, despite this widely use, there are few controlled studies confirming its biological activity in central nervous system.Materials and methods
The anxiolytic-like activity of the EO was investigated in light/dark box (LDB) and marble-burying test (MBT) and the antidepressant activity was investigated in forced-swimming test (FST) in mice. Flumazenil, a competitive antagonist of benzodiazepine binding and the selective 5-HT1A receptor antagonist WAY100635 was used in experimental procedures to determine the action mechanism of EO. To exclude any false positive results in experimental procedures, mice were submitted to the rota-rod test. We also quantified some neurotransmitters at specific brain regions after EO oral acute treatment.Results
The present work found anxiolytic-like activity of the EO at the dose of 10 mg/kg in a LDB. Flumazenil, but not WAY100635, was able to reverse the effect of the EO in the LDB, indicating that the EO activity occurs via the GABAA receptor-benzodiazepine complex. Only at higher doses did the EO potentiate diethyl-ether-induced sleeping time in mice. In the FST and MBT, EO showed no effect. Finally, the increase in time spent in the light chamber, demonstrated by concomitant treatment with ineffective doses of diazepam (DZP) and the EO, revealed a synergistic effect of the two compounds. The lack of activity after long-term treatment in the LDB test might be related to tolerance induction, even in the DZP-treated group. Furthermore, there were no significant differences between groups after either acute or repeated treatments with the EO in the rota-rod test. Neurochemical evaluation showed no amendments in neurotransmitter levels evaluated in cortex, striatum, pons, and hypothalamus.Conclusions
The results corroborate the use of Cymbopogon citratus in folk medicine and suggest that the anxiolytic-like effect of its EO is mediated by the GABAA receptor-benzodiazepine complex. 相似文献15.
我院门诊镇静催眠药应用情况分析 总被引:4,自引:0,他引:4
目的:了解我院门诊处方镇静催眠药的应用情况。方法:随机抽取我院2008年3月49791张门诊处方中镇静催眠药处方1317张,分析应用频次排序列前5位药物的用药合理性。结果:应用频次列前5位的镇静催眠药分别为阿普唑仑片、艾司唑仑片(舒乐安定)、劳拉西泮片(罗拉)、唑吡坦片(思诺思)和氯硝西泮片,其药物利用指数值分别为0.54、0.73、0.19、0.81及0.53。结论:我院镇静催眠药应用剂量较合理,与药品说明书所列适应证的相符率较高。 相似文献
16.
17.
《Neurological research》2013,35(8):804-812
AbstractObjectives: The aim of this study was to investigate the effects of oral administration of a novel benzodiazepine derivative, JM-20, on the neurological behavior of different rodent models, focusing on the GABAergic effect. We have also investigated the acute toxicity of oral administration of JM-20 in mice.Methods: Mice or rats received oral administration of JM-20 at 2, 4, 8, and 10 mg/kg to evaluate the sedative/hypnotic, anxiolytic, and anticonvulsant effects, as well as the influence on the stereotyped behavior induced by amphetamine. Diazepam (DZP) was used as a positive control. In addition, the mice received a single oral JM-20 dose of 2000 mg/kg to evaluate the acute toxicity.Results: In a dose-dependent manner, JM-20 (i) increased the number of crossings and decreased the number of rearings in the open-field test; (ii) decreased the aggressive behavior of socially-isolated mice; and (iii) increased the latency period for tonic seizure’s onset and the percentage of survival of animals with seizures. Moreover, JM-20 increased the sleeping time induced by barbiturates and the time spent and the number of entries in the open arms of the elevated plus-maze test. In the JM-20 toxicity test, no mortality was observed and only minor signs of toxicity associated with sedation were detected.Conclusions: These results indicate that JM-20 has an anxiolytic profile similar to DZP and its dihydropyridine moiety did not appear to interfere with the GABAergic activity associated with benzodiazepine. Furthermore, JM-20 did not show significant acute toxic effects in mice. 相似文献
18.
19.
20.
Evaluation of the discriminative stimulus effects of the novel sedative-hypnotic CL 284,846 总被引:2,自引:0,他引:2
CL 284,846,N-[3-(3-cyanopyrazolo[1, 5-a]pyrimidin-7-yl)phenyl)]-N-ethylacetamide, is a novel non-benzodiazepine sedative-hypnotic with benzodiazepine-like sedative effects, but with less apparent liability for accompanying undesired side effects. In an effort to further characterize its pharmacological activity, CL 284,846 (3.0 mg/kg, IP, 30 min pretreatment) was established as a discriminative stimulus (DS) in rats (n=7). CL 284,846 (0.3–10.0 mg/kg) showed a dose-related increase in drug-appropriate responding up to the training dose and a dose-related decrease in response rate. The benzodiazepine agonist triazolam (0.1–1.0 mg/kg), the benzodiazepine partial agonist Ro 17-1812 (0.3–3.0 mg/kg) and the triazolopyridazine CL 218,872 (1.0–3.0 mg/kg) substituted for CL 284,846 in all rats, whereas the imidazopyridines zolpidem (3.0–10.0 mg/kg) and alpidem (10.0–30.0 mg/kg), the benzodiazepine partial agonist bretazenil (0.03–10.0 mg/kg) and the novel putative anxiolytic CL 273,547 (10.0–56.0 mg/kg) substituted in most, but not all, rats. Ro 17-1812, bretazenil, and CL 218,872 had no effect on response rate while the other drugs showed a concomitant decrease in rate. The 5-HT1A agonist buspirone (1.0–10.0 mg/kg) and the barbiturate pentobarbital (3.0–17.0 mg/kg) failed to substitute for CL 284,846 up to rate-decreasing doses. The benzodiazepine antagonist flumazenil (3.0–10.0 mg/kg) blocked the DS effects of CL 284,846 in most rats with no effect on response rate. Taken together, these results suggest that the DS effects of CL 284,846 are mediated via benzodiazepine receptors; however, the DS profile of CL 284,846 remains distinct from both benzodiazepine and non-benzodiazepine sedative-hypnotic drugs. 相似文献