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991.
Yue Sheng Bo Sun Wen-Ting Guo Xiao Liu Yu-Chun Wang Xin Xie Xiao-Lin Xiao Na Li De-Li Dong 《British journal of pharmacology》2014,171(21):4970-4980
Background and Purpose
Autophagy is an important intracellular degradation system, which is related to various diseases. In preliminary experiments we found that D4-[6-(4-isopropoxyphenyl)pyrazolo [1,5-a]pyrimidin-3-yl] quinoline (DMH1) inhibited autophagy responses. However DMH1 also inhibits the signalling pathway activated by bone morphogenetic protein-4 (BMP4). The aim of the present study was to elucidate the inhibitory effects of DMH1 on autophagy and the underlying mechanisms.Experimental Approach
The effects of DMH1 on autophagy responses were evaluated in cultures of different cell types and with different stimuli to induce autophagy, using Western blots, transmission electron microscopy and fluorescent microscopy.Key Results
DMH1 inhibited starvation-induced autophagy in cardiomyocytes, HeLa and MCF-7 cells, without involving the signalling pathway of BMP4. DMH1 inhibited aminoimidazole carboxamide ribonucleotide (AICAR)- and rapamycin-induced autophagy in HeLa and MCF-7 cells. DMH1 reversed starvation- and AICAR-induced inhibition of Akt, mammalian target of rapamycin (mTOR) and p70S6 kinase (S6K), and reversed rapamycin-induced inhibition of mTOR and S6K. DMH1 reversed starvation-induced decrease of the phosphorylated form of glycogen synthase kinase-3 in MCF-7 and HT29 cells. Activation of Akt and inhibition of autophagy induced by DMH1 were antagonized by an Akt specific inhibitor or by small interfering RNA for Akt in HeLa cells.Conclusion and Implications
DMH1 inhibited cellular autophagy responses in a range of cell types and the underlying mechanisms include activation of the Akt pathway. 相似文献992.
Benjamin L. Woolbright Feng Li Yuchao Xie Anwar Farhood Peter Fickert Michael Trauner Hartmut Jaeschke 《Toxicology letters》2014
Lithocholic acid (LCA) supplementation in the diet results in intrahepatic cholestasis and bile infarcts. Previously we showed that an innate immune response is critical for cholestatic liver injury in the bile duct ligated mice. Thus, the purpose of this study was to investigate the role of neutrophils in the mechanism of liver injury caused by feeding mice a diet containing LCA. C57BL/6 mice were given control or 1% LCA containing diet for 24–96 h and then examined for parameters of hepatotoxicity. Plasma ALT levels were significantly increased by 48 h after LCA feeding, which correlated with both neutrophil recruitment to the liver and upregulation of numerous pro-inflammatory genes. The injury was confirmed by histology. Deficiency in intercellular adhesion molecule-1 (ICAM-1) expression or inhibition of neutrophil function failed to protect against the injury. Bile acid levels were quantified in plasma and bile of LCA-fed mice after 48 and 96 h. Only the observed biliary levels of taurochenodeoxycholic acid and potentially tauro-LCA caused direct cytotoxicity in mouse hepatocytes. These data support the conclusion that neutrophil recruitment occurs after the onset of bile acid-induced necrosis in LCA-fed animals, and is not a primary mechanism of cell death when cholestasis occurs through accumulation of hydrophobic bile acids. 相似文献
993.
Weidong Zhang Fengliang Wang Pengfei Xu Chen Miao Xin Zeng Xianwei Cui Cheng Lu Hui Xie Hong Yin Fei Chen Jingjing Ma Sheng Gao Ziyi Fu 《Toxicology letters》2014
Perfluorooctanoic acid (PFOA) is widely used because of its stain-resistant and water-repellant properties. This study aimed to explore the molecular mechanisms undergoing the stimulation effects of PFOA on cancer cell invasion and matrix metalloproteinases (MMPs) expression. Trans-well filter assay showed that PFOA exposure (≥5 nM) evidently enhanced the invasion ability of the breast cancer cells MDA-MB-231. Luciferase reporter assay, quantitative real-time PCR, western blotting and gelatin zymography consistently demonstrated that mRNA and protein levels of MMP-2/-9 were increased in the cells after PFOA treatment (P < 0.05 each). Western blotting revealed that PFOA could activate nuclear factor kappaB (NF-κB) by accelerating NF-κB translocation into the nucleus. Furthermore, addition of NF-κB inhibitor in culture medium could suppress the breast cancer cells invasiveness enhancement and MMP-2/-9 overexpression. This study indicates that PFOA can stimulate breast cancer cells invasion and up-regulate matrix metalloproteinase-2/-9 expression mediated by activating NF-κB, which deserves more environmental health concerns. 相似文献
994.
Xiang-Quan Xie Kui-Cheng Zheng Bing-Shan Wu Tie-Hui Chen Shan-Rong Lai Zai-Sheng Lin Kazuo Aoki 《Yebang Ŭihakhoe chi》2014,47(5):281-287
Objectives:
In Fujian Province, China, gastric cancer is one of the leading causes of mortality among all malignant tumors. Nanjing county and Minqing county are located in inland Fujian and have similar general demographics. However, the adjusted mortality rate of gastric cancer in Minqing was found to be much higher than that in Nanjing. We sought to explore factors associated with this increased risk of gastric cancer between the two counties.Methods:
We recruited 231 and 224 residents from Nanjing and Minqing, respectively, and analyzed differences between their dietary habits, Helicobacter pylori infection rates, and concentrations of serum pepsinogen I, pepsinogen II, gastrin-17, and ratio of pepsinogen I:II.Results:
Subjects in Minqing had more first-degree relatives who had been diagnosed with upper gastrointestinal tumor, more unhealthy dietary habits, a higher Helicobacter pylori positive rate, and greater proportion of abnormal serum gastrin-17 than those in Nanjing did.Conclusions:
The factors that differed between these two counties might indicate that residents in Minqing have a higher risk for developing gastric cancer than those in Nanjing do. 相似文献995.
Heather C Lasseter Xiaohu Xie Amy A Arguello Audrey M Wells Matthew A Hodges Rita A Fuchs 《Neuropsychopharmacology》2014,39(3):660-669
Cocaine-seeking behavior triggered by drug-paired environmental context exposure is dependent on orbitofrontal cortex (OFC)–basolateral amygdala (BLA) interactions. Here, we present evidence supporting the hypothesis that dopaminergic input from the ventral tegmental area (VTA) to the OFC critically regulates these interactions. In experiment 1, we employed site-specific pharmacological manipulations to show that dopamine D1-like receptor stimulation in the OFC is required for drug context-induced reinstatement of cocaine-seeking behavior following extinction training in an alternate context. Intra-OFC pretreatment with the dopamine D1-like receptor antagonist, , dose-dependently attenuated cocaine-seeking behavior in an anatomically selective manner, without altering motor performance. Furthermore, the effects of SCH23390 could be surmounted by co-administration of a sub-threshold dose of the D1-like receptor agonist, SCH23390. In experiment 2, we examined effects of D1-like receptor antagonism in the OFC on OFC-BLA interactions using a functional disconnection manipulation. Unilateral SKF81297 administration into the OFC plus GABA agonist-induced neural inactivation of the contralateral or ipsilateral BLA disrupted drug context-induced cocaine-seeking behavior relative to vehicle, while independent unilateral manipulations of these brain regions were without effect. Finally, in experiment 3, we used fluorescent retrograde tracers to demonstrate that the VTA, but not the substantia nigra, sends dense intra- and interhemispheric projections to the OFC, which in turn has reciprocal bi-hemispheric connections with the BLA. These findings support that dopaminergic input from the VTA, via dopamine D1-like receptor stimulation in the OFC, is required for OFC–BLA functional interactions. Thus, a VTA–OFC–BLA neural circuit promotes drug context-induced motivated behavior. SCH23390相似文献
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999.
目的建立复方枇杷桔梗膏的质量标准。方法采用薄层色谱(TLC)法对复方枇杷桔梗膏中的枇杷叶、罂粟壳、桔梗和薄荷脑进行定性鉴别,以高效液相色谱(HPLc)法对该制剂中的吗啡进行含量测定。结果复方枇杷桔梗膏中枇杷叶、罂粟壳、桔梗和薄荷脑的TLC中,在与对照药材溶液色谱相应位置上显相同颜色的斑点;吗啡进样量在0.0204~1.023txg范围内与峰面积线性关系良好(r=0.9997),平均回收率为99.09%,RSD为1.40%(n=6)。结论该方法简便、准确、灵敏、重复性好,可用于该制剂的质量控制。 相似文献
1000.
目的观察甲氨蝶呤联合强的松治疗类风湿关节炎(RA)的效果和并发症,并探讨护理策略。方法选取2012年1月至2013年10月收治的RA患者100例,随机分为观察组和对照组,各50例。对照组应用甲氨蝶呤治疗,观察组应用甲氨蝶呤联合强的松治疗。观察两组患者的疗效,治疗后平均红细胞沉降率(ESR)、C蛋白反应(CRP)、类风湿因子(RF),平均晨僵、握力及不良反应。结果观察组显效率为44.00%,明显高于对照组的34.00%(P<0.05);观察组无效率为4.00%,明显低于对照组的12.00%(P<0.05);观察组治疗后晨僵(2.21±0.08)h,明显低于对照组的(2.57±0.10)h(P<0.05);观察组治疗后握力为(12.85±0.41)kPa,高于对照组的(10.69±0.58)kPa(P<0.05);观察组治疗后平均ESR,CRP,RF滴度分别为(24.36±0.93)mm/h,(11.22±0.48)mg/L,11.53±0.40,均明显低于对照组治疗后的(28.71±1.48)mm/h,(13.15±0.50)mg/L,14.07±0.68(P<0.05)。两组主要不良反应发生率比较,无统计学差异。结论甲氨蝶呤联合强的松治疗RA疗效显著,患者的症状和主要指标均有明显改善,合理的护理措施亦有助于患者病情的缓解。 相似文献