全文获取类型
收费全文 | 31227篇 |
免费 | 2561篇 |
国内免费 | 279篇 |
专业分类
耳鼻咽喉 | 318篇 |
儿科学 | 1082篇 |
妇产科学 | 705篇 |
基础医学 | 3631篇 |
口腔科学 | 640篇 |
临床医学 | 2991篇 |
内科学 | 6637篇 |
皮肤病学 | 552篇 |
神经病学 | 2403篇 |
特种医学 | 1032篇 |
外科学 | 4682篇 |
综合类 | 828篇 |
一般理论 | 14篇 |
预防医学 | 2064篇 |
眼科学 | 1310篇 |
药学 | 2384篇 |
1篇 | |
中国医学 | 131篇 |
肿瘤学 | 2662篇 |
出版年
2023年 | 217篇 |
2022年 | 344篇 |
2021年 | 738篇 |
2020年 | 473篇 |
2019年 | 696篇 |
2018年 | 802篇 |
2017年 | 568篇 |
2016年 | 657篇 |
2015年 | 753篇 |
2014年 | 1029篇 |
2013年 | 1215篇 |
2012年 | 1985篇 |
2011年 | 2045篇 |
2010年 | 1181篇 |
2009年 | 1033篇 |
2008年 | 1789篇 |
2007年 | 1800篇 |
2006年 | 1620篇 |
2005年 | 1560篇 |
2004年 | 1548篇 |
2003年 | 1371篇 |
2002年 | 1225篇 |
2001年 | 1138篇 |
2000年 | 1032篇 |
1999年 | 884篇 |
1998年 | 319篇 |
1997年 | 260篇 |
1996年 | 224篇 |
1995年 | 221篇 |
1994年 | 195篇 |
1993年 | 175篇 |
1992年 | 519篇 |
1991年 | 483篇 |
1990年 | 443篇 |
1989年 | 415篇 |
1988年 | 369篇 |
1987年 | 340篇 |
1986年 | 331篇 |
1985年 | 330篇 |
1984年 | 224篇 |
1983年 | 207篇 |
1982年 | 140篇 |
1981年 | 105篇 |
1980年 | 112篇 |
1979年 | 161篇 |
1978年 | 93篇 |
1977年 | 103篇 |
1976年 | 70篇 |
1974年 | 85篇 |
1973年 | 71篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
991.
992.
993.
994.
995.
Alyssa M. Civantos Yasmeen Byrnes Changgee Chang Aman Prasad Kevin Chorath Seerat K. Poonia Carolyn M. Jenks Andrs M. Bur Punam Thakkar Evan M. Graboyes Rahul Seth Samuel Trosman Anni Wong Benjamin M. Laitman Brianna N. Harris Janki Shah Vanessa Stubbs Garret Choby Qi Long Christopher H. Rassekh Erica Thaler Karthik Rajasekaran 《Head & neck》2020,42(7):1597-1609
996.
J. K. Jewer M. J. Wong S. J. Bird A. S. Habib R. Parker R. B. George 《Anaesthesia》2020,75(2):254-265
We conducted a Cochrane systematic review on the effectiveness of supplemental intravenous crystalloid administration in preventing postoperative nausea and vomiting. We included randomised controlled trials of patients undergoing surgery under general anaesthesia and given supplemental peri-operative intravenous crystalloid. Our primary outcomes were the risk of postoperative nausea and the risk of postoperative vomiting. We assessed the risk of bias for each included study and applied the Grading of Recommendations, Assessment, Development and Evaluations (GRADE) framework for the certainty of evidence. We included 41 studies. We found that the intervention probably reduces the overall risk of postoperative nausea, the risk ratio (95%CI) being 0.62 (0.51–0.75) (I2 = 57%, p < 0.00001, 18 studies; 1766 participants; moderate-certainty evidence). It also probably reduces the risk of postoperative nausea within 6 h of surgery, with a risk ratio (95%CI) of 0.67 (0.58 to 0.78) (I2 = 9%, p < 0.00001, 20 studies; 2310 participants; moderate-certainty evidence) and by around 24 h, the risk ratio (95%CI) being 0.47 (0.32–0.69) (I2 = 38%, p = 0.0001, 17 studies; 1682 participants; moderate-certainty evidence). Supplemental intravenous crystalloid probably also reduces the overall risk of postoperative vomiting, with a risk ratio (95%CI) of 0.50 (0.40–0.63) (I2 = 31%, p < 0.00001, 20 studies; 1970 participants; moderate-certainty evidence). The beneficial effect on vomiting was seen both within 6 h and by around 24 h postoperatively. 相似文献
997.
The present study was undertaken to examine the effect of amitriptyline on the antinociceptive effect of morphine and its underlying mechanisms in regulating glutamate transporters trafficking in morphine-tolerant rats. Long-term morphine infusion induced antinociceptive tolerance and down-regulation of glutamate transporters (GTs), GLAST, GLT-1, and EAAC1, expression in the rat spinal cord dorsal horn. Acute amitriptyline treatment potentiated morphine’s antinociceptive effect, with a 5.3-fold leftward shift of morphine’s dose–response curve in morphine-tolerant rats, and this was associated with GLAST and GLT-1 trafficking onto the cell surface. Similar to our previous studies, morphine challenge (10 μg/10 μl, i.t.) significant by increased the excitatory amino acids (EAAs) aspartate and glutamate level in the CSF dialysates of morphine-tolerant rats. Acute amitriptyline treatment not only suppressed this morphine-evoked EAA release, but further reduced the EAA concentration than baseline level. Furthermore, long-term morphine infusion up-regulated PKA and PKC protein expression in the spinal cord dorsal horn, while amitriptyline inhibited the increase in expression of phospho-PKA, PKCα, PKCβII, and PKCγ. In morphine-tolerant rats, acute treatment with PKA inhibitor H89 and PKC inhibitor Gö6805 attenuated morphine tolerance and the morphine-induced CSF glutamate and aspartate elevation, and induced trafficking of GLAST and GLT-1 from cytosol onto the cell surface. These results show that acute amitriptyline treatment preserved morphine’s antinociceptive effect in morphine-tolerant rats; the mechanisms may be involved in inhibition of phospho-PKA and PKC expression, and thus inducing the GLAST and GLT-1 trafficking onto glial cell surface which enhances the EAA uptake from the synaptic cleft and reduces EAA concentration in the spinal CSF. 相似文献
998.
999.
Li YW Hill G Wong H Kelly N Ward K Pierdomenico M Ren S Gilligan P Grossman S Trainor G Taub R McElroy J Zazcek R 《The Journal of pharmacology and experimental therapeutics》2003,305(1):86-96
4-(1,3-Dimethoxyprop-2-ylamine)-2,7-dimethyl-8-(2,4-dichlorophenyl)-pyrazolo[1,5-a]-1,3,5-triazine (DMP696) is a highly selective and potent, nonpeptide corticotropin-releasing factor 1 (CRF(1)) antagonist. In this study, we measured in vivo CRF(1) receptor occupancy of DMP696 by using ex vivo ligand binding and quantitative autoradiography and explored the relationship of receptor occupancy with plasma and brain exposure and behavioral efficacy. In vitro affinity (IC(50)) of DMP696 to brain CRF(1) receptors measured using the brain section binding autoradiography in this study is similar to that assessed using homogenized cell membrane assays previously. The ex vivo binding assay was validated by demonstrating that potential underestimation of receptor occupancy with this procedure could be minimized by identifying an appropriate in vitro incubation time (40 min) based upon the dissociation kinetics of DMP696. Orally administrated DMP696 dose dependently occupied CRF(1) receptors in the brain, with ~60% occupancy at 3 mg/kg. In the defensive withdrawal test of anxiety, this dose of DMP696 produced approximately 50% reduction in the exit latency. The time course of plasma and brain drug levels paralleled that of receptor occupancy, with peak exposure at 90 min after dosing. The plasma-free concentration of DMP696 corresponding to 50% CRF(1) receptor occupancy (in vivo IC(50), 1.22 nM) was similar to the in vitro IC(50) (~1.0 nM). Brain concentrations of DMP696 were over 150-fold higher than the plasma-free levels. In conclusion, doses of DMP696 occupying over 50% brain CRF(1) receptors are consistent with doses producing anxiolytic efficacy in the defense withdrawal test of anxiety, and the IC(50) value estimated in vivo based on plasma-free drug concentrations is consistent with the in vitro IC(50) value. 相似文献
1000.
Jun Deguchi Kaori Horiguchi Chin Piow Wong Takahiro Hosoya Akane Iihoshi Toshio Kaneda Hiroshi Morita 《Journal of natural medicines》2014,68(4):723-729
Previously, we reported the isolation of cassane-type diterpenes, sucutiniranes A–F, from the seeds of Bowdichia nitida. In this study, a series of sucutinirane derivatives was prepared, and their in vitro toxicity in the HL-60 cell line was evaluated. Then the action mechanism of a representative compound that induces cell death was investigated. Whereas C-6 or C-7 diol esters and ether decreased the activity against the HL-60 cell line, furan-oxidized derivatives 12 and 13 showed improvement or retention of the activity compared with those of the natural products sucutinirane A (11), E (1), and F (2). Treatment with sucutinirane derivative 13 elevated caspase 3/7 activity and also decreased expression of Bcl-2 family proteins, Mcl-1, and Bid. Derivative 13 generated reactive oxygen species in HL-60 cells, whose apoptotic effects were attenuated by the addition of an antioxidant, N-acetyl-l-cysteine. These results suggest that cassane butenolide 13 induces apoptosis in HL-60 via its oxidative effects. 相似文献