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51.
Scutellariae radix (SR) is an herbal medicine used for the treatment of inflammatory diseases. To investigate whether the SR water extract has a hepatoprotective effect in mice fed a high fat diet with chronic alcohol consumption, ICR mice were fed one of the following diets: a control diet (CD, 16% fat), a high fat diet (HFD, 40% fat), a high fat diet with either ethanol (HFDE, 25% v/v, ad libitum) alone or ethanol with SR extract (HFDESR, 100 mg/kg, p.o.) for 28 days, respectively. The combination of high fat diet with ethanol exposure induced hepatic damage that was manifested by a significant increase in the activities of functional enzymes, alanine transaminase (ALT), aspartate transaminase (AST) and lactate dehydrogenase (LDH) in serum. Also, the liver and visceral fat weights were increased and the lipid profiles in serum and liver homogenate including triglyceride, total cholesterol, LDL‐cholesterol were significantly deteriorated. The SR supplements significantly reversed these altered parameters to near the values of the CD mice. Specifically, the expression of 3‐hydroxy‐3‐methylglutaryl‐coenzymeA (HMG‐CoA) reductase in liver homogenate was significantly lowered in the HFDESR group compared with that of either the HFD or HFDE groups, which revealed that the SR extract could afford protection in the alleviation of high fat and alcoholic liver damage. Copyright © 2011 John Wiley & Sons, Ltd. 相似文献
52.
Ku‐aida Tuansulong Nongporn Hutadilok‐Towatana Wilawan Mahabusarakam Decha Pinkaew Ken Fujise 《Phytotherapy research : PTR》2011,25(3):424-428
Morelloflavone, a biflavonoid from Garcinia dulcis previously shown to have hypocholesterolemic activity, was examined for its effect on HMG‐CoA reductase, the rate‐limiting enzyme of the cholesterol biosynthetic pathway. By using the catalytic domain of house mouse HMG‐CoA reductase, morelloflavone was found to inhibit the enzyme activity by competing with HMG‐CoA whereas it was non‐competitive towards NADPH. The inhibition constants (Ki) with respect to HMG‐CoA and NADPH were 80.87 ± 0.06 µm and 103 ± 0.07 µm , respectively. Both flavonoid subunits of this compound, naringenin and luteolin, equally competed with HMG‐CoA with Ki of 83.58 ± 4.37 µm and 83.59 ± 0.94 µm , respectively, and were also non‐competitive with NADPH (Ki of 182 ± 0.67 µm and 188 ± 0.14 µm , respectively). Due to these findings, we suggest that each subunit of morelloflavone would occupy the active site of the enzyme, thereby blocking access of its substrate. The present study thus demonstrates the ability of morelloflavone from G. dulcis to inhibit HMG‐CoA reductase in vitro. As a result, this biflavonoid might serve as a new candidate for the future development of hypocholesterolemic agents. Copyright © 2010 John Wiley & Sons, Ltd. 相似文献
53.
目的:探讨乙酰辅酶A羧化酶抑制剂TOFA对卵巢癌COC1细胞增殖能力的抑制作用及其机制。方法:采用细胞增殖/毒性检测试剂(CCK-8)检测不同浓度TOFA作用24、48、72h对卵巢癌细胞增殖抑制作用,流式细胞仪检测COC1的细胞周期变化情况,免疫印迹技术(Western blot)检测COC1细胞磷酸化AKT、ERK蛋白表达的变化。结果:不同浓度(1、5、10、20、50μg/ml)TOFA分别作用24、48、72h后,对卵巢癌细胞的增殖抑制作用呈时间和剂量依赖。5、10、20、50μg/ml TOFA处理48h后实验组和对照组相比,阻滞于G0/G1期的细胞数明显增加(P<0.05)。10μg/ml TOFA作用后,可上调磷酸化AKT蛋白表达,60min后磷酸化ERK蛋白表达抑制率为47%(P>0.05)。结论:TOFA对卵巢癌细胞增殖抑制作用呈时间和剂量依赖性,诱导细胞G0/G1期阻滞,抑制磷酸化ERK表达,TOFA发挥作用的机制可能与MAPK/ERK信号转导通路相关。 相似文献
54.
Nagasawa M Akasaka Y Ide T Hara T Kobayashi N Utsumi M Murakami K 《Biochemical pharmacology》2007,74(12):1738-1746
Peroxisome proliferator-activated receptor alpha (PPARalpha) is a key regulator in hepatic lipid metabolism and a potential therapeutic target for dyslipidemia. However, in humans hepatic PPARalpha-regulated genes remain unclear. To investigate the effect of PPARalpha agonism on mRNA expressions of lipid metabolism-related genes in human livers, a potent PPARalpha agonist, KRP-101 (KRP), was used to treat the human hepatoma cell line, HepaRG cells. KRP did not affect AOX or L-PBE, which are involved in peroxisomal beta-oxidation. KRP increased L-FABP, CPT1A, VLCAD, and PDK4, which are involved in lipid transport or oxidation. However, the EC(50) values (114-2500 nM) were >10-fold weaker than the EC(50) value (10.9 nM) for human PPARalpha in a transactivation assay. To search for more sensitive genes, we determined the mRNA levels of apolipoproteins, apoA-I, apoA-II, apoA-IV, apoA-V, and apoC-III. KRP had no or little effect on apoA-I, apoC-III, and apoA-II. Interestingly, KRP increased apoA-IV (EC(50), 0.99 nM) and apoA-V (EC(50), 0.29 nM) with high sensitivity. We identified apoA-IV as a PPARalpha-upregulated gene in a study using PPARalpha siRNA. Moreover, when administered orally to dogs, KRP decreased the serum triglyceride level and increased the serum apoA-IV level in a dose-dependent manner. These findings suggest that apoA-IV, newly identified as a highly sensitive PPARalpha-regulated gene in human livers, may be one of the mechanisms underlying PPARalpha agonist-induced triglyceride decrease and HDL elevation. 相似文献
55.
Browning DR Martin RM 《International journal of cancer. Journal international du cancer》2007,120(4):833-843
We conducted a systematic review of the association between HMG-CoA reductase inhibitor (statin) use and cancer risk. We searched MEDLINE, EMBASE, Web of Science, ISI Proceedings and BIOSIS Previews bibliographic databases, electronic trials registers and reference lists for potentially eligible randomized trials and observational studies. Thirty-eight individual studies (26 randomized trials involving 103,573 participants and 12 observational studies with 826,854 participants) were included. Median follow-up was 3.6 and 6.2 years for trials and observational studies, respectively. In metaanalyses of randomized trials, there was no evidence that statin therapy was associated with incidence of all-cancers (26 trials; pooled risk ratio = 1.00; 95% CI 0.95-1.05; I(2) = 0%) or the following site-specific cancers: breast (7 trials; risk ratio = 1.01; 0.79-1.30; I(2) = 43%), prostate (4 trials; risk ratio = 1.00; 0.85-1.17; I(2) = 0%), colorectum (9 trials; risk ratio = 1.02; 0.89-1.16; I(2) = 0%), lung (9 trials; risk ratio = 0.96; 0.84-1.09; I(2) = 0%), genito-urinary (5 trials; risk ratio = 0.95; 0.83-1.09; I(2) = 0%), melanoma (4 trials; risk ratio = 0.86; 0.62-1.20; I(2) = 17%) or gastric (1 trial; risk ratio = 1.00; 0.35-2.85). There was no evidence of differential effects by length of follow-up, statin type (lipophilic vs. lipophobic) or potency. Trial results were generally consistent with observational studies. We conclude that statin use is not associated with short-term cancer risk, but longer-latency effects remain possible. 相似文献
56.
A known risk factor for the development of coronary artery disease and subsequent myocardial infarction is hypercholesterolaemia. The widespread nature of this phenomenon in the western world has led to the development of agents which reduce serum cholesterol levels. One such class of agents, HMG‐CoA reductase inhibitors (statins) are very effective in cholesterol reduction. Recently, clinical and experimental evidence has amassed suggesting that patients taking statins receive cardiovascular benefits that occur independent of cholesterol reduction. Experimental data suggest that statins may increase levels of nitric oxide (NO) in vivo. This review will address the ‘cholesterol‐independent’ vasculoprotective and cardioprotective effects of statins in animal models. Upon completion, the reader will be familiar with the proposed cholesterol‐independent pathways of statins and understand that the cholesterol‐independent benefits may arise from enhanced production of NO. 相似文献
57.
58.
药用植物功能基因的研究思路与展望——以甘草为例 总被引:1,自引:0,他引:1
近些年来有关功能基因的研究已成为药用植物研究领域的热点,研究内容涉及基因克隆、功能鉴定、多态性分析、表达模式分析以及功能基因与代谢途径的相关性分析等诸多方面。甘草是我国最常用的大宗药材之一,其主要活性成分为甘草酸,具有多种药理功能,在国内外市场上应用广泛。本文以甘草为例,对甘草酸代谢途径中已报道的功能基因进行调查研究,在基因克隆、基因功能、基因多态性等方面进行分析,以期为揭示甘草酸合成代谢的分子机制奠定基础,并为其他药用植物功能基因的研究提供思路。 相似文献
59.