全文获取类型
收费全文 | 1361篇 |
免费 | 123篇 |
国内免费 | 37篇 |
专业分类
儿科学 | 7篇 |
妇产科学 | 7篇 |
基础医学 | 50篇 |
口腔科学 | 2篇 |
临床医学 | 93篇 |
内科学 | 75篇 |
皮肤病学 | 1篇 |
神经病学 | 501篇 |
特种医学 | 12篇 |
外科学 | 14篇 |
综合类 | 52篇 |
预防医学 | 34篇 |
眼科学 | 1篇 |
药学 | 551篇 |
中国医学 | 108篇 |
肿瘤学 | 13篇 |
出版年
2023年 | 11篇 |
2022年 | 27篇 |
2021年 | 30篇 |
2020年 | 30篇 |
2019年 | 41篇 |
2018年 | 42篇 |
2017年 | 49篇 |
2016年 | 43篇 |
2015年 | 58篇 |
2014年 | 67篇 |
2013年 | 153篇 |
2012年 | 72篇 |
2011年 | 89篇 |
2010年 | 76篇 |
2009年 | 73篇 |
2008年 | 81篇 |
2007年 | 49篇 |
2006年 | 56篇 |
2005年 | 48篇 |
2004年 | 36篇 |
2003年 | 40篇 |
2002年 | 35篇 |
2001年 | 33篇 |
2000年 | 13篇 |
1999年 | 9篇 |
1998年 | 12篇 |
1997年 | 24篇 |
1996年 | 21篇 |
1995年 | 16篇 |
1994年 | 15篇 |
1993年 | 9篇 |
1992年 | 13篇 |
1991年 | 12篇 |
1990年 | 12篇 |
1989年 | 8篇 |
1988年 | 13篇 |
1987年 | 8篇 |
1986年 | 5篇 |
1985年 | 11篇 |
1984年 | 14篇 |
1983年 | 10篇 |
1982年 | 15篇 |
1981年 | 12篇 |
1980年 | 11篇 |
1979年 | 3篇 |
1978年 | 2篇 |
1977年 | 4篇 |
1976年 | 2篇 |
1973年 | 3篇 |
1972年 | 3篇 |
排序方式: 共有1521条查询结果,搜索用时 15 毫秒
41.
42.
43.
44.
《The world journal of biological psychiatry》2013,14(6):412-431
AbstractObjectives. The treatment of major affective disorders, commonly associated with high disability and elevated social costs may be still considered unsatisfactory. Among all antidepressant drugs, predominantly acting through monoaminergic mechanisms, agomelatine is of particular interest due to another alternative mechanism of action. Targeting melatonergic receptors, agomelatine play a crucial role in synchronizing circadian rhythms, known to be altered in depressed subjects. Methods. A critical review of the literature focusing on efficacy, safety and tolerability of agomelatine in major affective disorders was performed. Additionally, we focused on the potential of agomelatine in enhancing neuroplasticity mechanisms and promote neurogenesis. A total of 136 articles from peer-reviewed journals were identified, of which 50 were assessed for eligibility and 21 were included. Results. Agomelatine, a melatonergic analogue drug acting as MT1/MT2 agonist and 5-HT2C antagonist, has been reported to be effective as antidepressant drug. Studies confirmed not only clinical efficacy but also safety and tolerability of agomelatine. Also, it enhances neuroplasticity mechanisms and adult neurogenesis in brain areas such as hippocampus and prefrontal cortex. Conclusions. Agomelatine actually represents an intriguing option in the treatment of affective disorders. 相似文献
45.
46.
B D Sachs J P R Jacobsen T L Thomas W B Siesser W L Roberts M G Caron 《Translational psychiatry》2013,3(8):e291
The importance of reversing brain serotonin (5-HT) deficiency and promoting hippocampal neurogenesis in the mechanisms of action for antidepressants remain highly controversial. Here we examined the behavioral, neurochemical and neurogenic effects of chronic fluoxetine (FLX) in a mouse model of congenital 5-HT deficiency, the tryptophan hydroxylase 2 (R439H) knock-in (Tph2KI) mouse. Our results demonstrate that congenital 5-HT deficiency prevents a subset of the signature molecular, cellular and behavioral effects of FLX, despite the fact that FLX restores the 5-HT levels of Tph2KI mice to essentially the levels observed in wild-type mice at baseline. These results suggest that inducing supra-physiological levels of 5-HT, not merely reversing 5-HT deficiency, is required for many of the antidepressant-like effects of FLX. We also demonstrate that co-administration of the 5-HT precursor, 5-hydroxytryptophan (5-HTP), along with FLX rescues the novelty suppressed feeding (NSF) anxiolytic-like effect of FLX in Tph2KI mice, despite still failing to induce neurogenesis. Thus, our results indicate that brain 5-HT deficiency reduces the efficacy of FLX and that supplementation with 5-HTP can restore some antidepressant-like responses in the context of 5-HT deficiency. Our findings also suggest that feeding latency reductions in the NSF induced by chronic 5-HT elevation are not mediated by drug-induced increments in neurogenesis in 5-HT-deficient animals. Overall, these findings shed new light on the impact of 5-HT deficiency on responses to FLX and may have important implications for treatment selection in depression and anxiety disorders. 相似文献
47.
Kazuko Sakata Joshua R. Mastin Sean M. Duke Meghan G. Vail Abigail E. Overacre Brittany E. Dong Shanker Jha 《The European journal of neuroscience》2013,37(11):1863-1874
Brain‐derived neurotrophic factor (BDNF) is implicated in the pathophysiology of major depression; mice lacking BDNF expression through promoter IV (BDNF‐KIV) exhibit a depression‐like phenotype. We tested our hypothesis that deficits caused by promoter IV deficiency (depression‐like behavior, decreased levels of BDNF, and neurogenesis in the hippocampus) could be rescued by a 3‐week treatment with different types of antidepressants: fluoxetine, phenelzine, duloxetine, or imipramine. Each antidepressant reduced immobility time in the tail suspension test without affecting locomotor activity in the open field test in both BDNF‐KIV and control wild type mice, except that phenelzine increased locomotor activity in wild type mice and anxiety‐like behavior in BDNF‐KIV mice. The antidepressant treatments were insufficient to reverse decreased BDNF levels caused by promoter IV deficiency. No antidepressant treatment increased the hippocampal progenitors of either genotype, whereas phenelzine decreased the surviving progenitors in both genotypes. The antidepressant treatments differently affected the dendritic extension of hippocampal immature neurons: fluoxetine and imipramine increased extension in both genotypes, duloxetine increased it only in BDNF‐KIV mice, and phenelzine decreased it only in wild type mice. Interestingly, a saline‐only injection increased neurogenesis and dendrite extensions in both genotypes. Our results indicate that the behavioral effects in the tail suspension test by antidepressants do not require promoter IV‐driven BDNF expression and occur without a detectable increase in hippocampal BDNF levels and neurogenesis but may involve increased dendritic reorganisation of immature neurons. In conclusion, the antidepressant treatment demonstrated limited efficacy; it partially reversed the defective phenotypes caused by promoter IV deficiency but not hippocampal BDNF levels. 相似文献
48.
目的:探讨抑郁症患者治疗前后血浆皮质醇水平的变化。方法:对160例抑郁症患者给予抗抑郁药治疗6周,分别于治疗前及治疗后进行汉密尔顿抑郁量表(HAMD)、汉密尔顿焦虑量表(HAMA)评估及血浆皮质醇水平检测。结果:本组治疗前后HAMD总分分别为(24.98±5.10)和(7.57±5.61);HAMA总分分别为(20.62±6.90)和(6.21±5.17);血浆皮质醇水平分别为(407.34±144.29)nmol/L和(354.64±137.13)nmol/L。治疗后HAMD总分、HAMA总分及血浆皮质醇水平较治疗前明显下降(P均<0.001);不同性别间血浆皮质醇水平差异无统计学意义(P>0.05);血浆皮质醇变化值与HAMD、HAMA减分率不相关(r=0.084,r=0.049;P均>0.05)。结论:抗抑郁药物治疗可显著降低抑郁症患者血浆皮质醇水平。 相似文献
49.
目的从环磷酸腺苷(c AMP)信号通路角度探讨复方柴归方超临界CO_2提取物的抗抑郁作用机制。方法采用慢性温和不可预知应激(CUMS)程序对大鼠进行造模,以高、中、低剂量复方柴归方超临界CO_2提取物及文拉法辛为干预药物,检测各组大鼠海马组织中c AMP、蛋白激酶A(PKA)、环磷酸腺苷反应原件结合蛋白(CREB)、脑源性神经生长因子(BDNF)水平及其相应m RNA水平。结果与对照组比较,模型组大鼠海马组织中c AMP、PKA、p-CREB、BDNF水平显著下降(P0.05、0.01),复方柴归方干预后,与模型组比较,各剂量组c AMP、PKA、p-CREB、BDNF水平均出现回调(P0.05、0.01);同时,模型组大鼠海马组织中酪氨酸激酶B(TrkB)、PKA、p-CREB、BDNF的m RNA水平显著下降(P0.05、0.01),复方柴归方干预后,与模型组相比,各剂量组Trk B、PKA、p-CREB、BDNF的m RNA水平均出现回调(P0.05、0.01)。结论复方柴归方超临界CO_2提取物可通过调控c AMP-PKA-CREB-BDNF信号通路发挥抗抑郁作用。 相似文献
50.