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31.
Zilberman M 《Acta biomaterialia》2005,1(6):680-624
Bioresorbable polymer films containing dexamethasone (DM) were prepared using a solution processing technique. Investigation of the films focused on cumulative DM release as affected by film morphology (drug location/dispersion in the film) and degradation processes. Two film structures were studied: A-type, a polymer film with large drug crystals located on the film’s surface, and B-type, a polymer film with small drug particles and crystals distributed within the bulk. The effect of the polymer’s degree of crystallinity on the drug release profile was also studied. Prototypical applications of these films are biodegradable medical support devices which combine mechanical support with drug release. In most of our studied systems the drug release profile from the film is determined mainly by both drug location/dispersion in the film and the polymer’s weight loss rate. All release profiles from A-type films exhibited a burst effect of approximately 30%, accompanied by a second release phase at a constant rate, whereas the release profiles from B-type films were determined mainly by the degradation profile of the host polymer, and did not exhibit any burst effect. A high degree of crystallinity is important for the current application, since good mechanical properties are required. This contributes to slower drug release rates, mainly at relatively low weight losses, whereas at high weight losses, where a porous structure is created, the crystallinity almost does not affect the rate of drug release. The shape of the porous structure that develops with degradation also affects the drug release profile from the B-type films. 相似文献
32.
人外周血树突状细胞培养和地塞米松对其分化的影响作用 总被引:1,自引:0,他引:1
目的分离培养和鉴定人外周血树突状细胞(DC),以及探讨地塞米松对其分化的影响作用。方法密度梯度离心法分离人外周血单个核细胞,贴壁后加入GM-CSF、IL-4和LPS培养,部分组另加入地塞米松,观察细胞形态学、流式标志和DC与T淋巴细胞共培养后的增殖变化。结果外周血单核细胞诱导培养后具有DC形态学特征,CD83表达上调,CD14表达下调,DC与T淋巴细胞共培养后呈增殖反应。培养液中加入地塞米松后CD83表达下调,CD14表达上调,DC与T淋巴细胞共培养后增殖反应减弱。结论外周血单核细胞经联合细胞因子可诱导为DC;地塞米松可使DC在功能上处于不成熟状态。 相似文献
33.
Failure to suppress cortisol secretion after administration of dexamethasone has been reported to be a diagnostic marker for major depression and to have prognostic implications when repeated after antidepressant treatment. The pulsatile pattern of cortisol secretion suggested to us that increasing the number of post-dexamethasone cortisol determinations might significantly increase the sensitivity of the dexamethasone suppression test (DST) for major depression. With a conventional two-point DST (1600 h and midnight), 5% of 20 normal volunteers, 8% of 13 inpatients with non-major depressions, and 31% of 65 inpatients with primary major depression failed to suppress. With six post-dexamethasone points (0800 h, 1200 h, 1600 h, 2000 h, 2200 h, midnight), the respective percentages were 10, 15 and 44%. The additional points increased the sensitivity from 31 to 44%, mostly by identifying more major depressives with a "late escape" pattern. If a clinician is using the DST to establish a marker for major depression that can be repeated to monitor response to treatment and the likelihood of relapse, then perhaps the increased sensitivity of the six-point DST would be helpful, despite a modest decrease in specificity from 94 to 88%. 相似文献
34.
地塞米松抑制小鼠腹腔巨噬细胞白细胞介素—18的表达 总被引:3,自引:1,他引:2
目的:研究糖皮质激素(GC)对小鼠腹腔巨噬细胞(Mφ)IL-18表达的调控作用。方法:以半定量RT-PCR法检测经不同浓度地塞米松(Dex)处理的Mφ脂多糖(LPS)诱导的IL-18mRNA的表达,以ELISA法检测Mφ培养上清IL-18的含量。结果:Dex剂量依赖性地抑制MφLPS诱导的IL-18mRNA及等抑制作用可被糖皮质激素受体拮抗剂-RU486阻断。结论:GC能抑制MφLPS诱导的IL-18的表达。 相似文献
35.
地塞米松诱导大鼠免疫细胞凋亡机制初探 总被引:12,自引:0,他引:12
报道了地塞米松诱导大鼠胸腺、脾细胞凋亡机制的初探。结果表明,地塞米松与这些器官的细胞共同培养不同时间,其糖皮质激素受体(GCR)量发生变化,胸腺细胞GCR量在培养1.5h组为67.72±15.21(fmol/106细胞),显著高于对照组30.57±8.25及5h组36.91±9.17(P<0.05),脾细胞GCR量各组差异不显著(P>0.05)。在细胞周期蛋白依赖抑制因子(ρ16)实验中,观察到P16阳性细胞数在1.5h组多于对照组及5h组。在形态学及生化实验中,对照组及1.5h组,胸腺、脾细胞Giemsa染色形态一致,其DNA未见断裂带;而5h组,胸腺:脾细胞可见核固缩、深染、核碎裂、体积小的凋亡细胞,其DNA电泳可见典型“梯状”条带。由此,推测地塞米松通过GCR的作用,影响细胞周期相关蛋白,进而诱导免疫细胞凋亡。 相似文献
36.
The production of biochemical markers associated with the osteoblastic phenotype, and accompanying changes in the expression of voltage-operated Ca2+ channels, have been examined in rat bone marrow stromal cell cultures treated with dexamethasone (10-8 M). Whole cell clamp analysis of voltage-operated Ca2+ channels in control cultures (using Ba2+ as the charge carrier) revealed primarily a high voltage-activated (HVA), slowly inactivating current, which was enhanced two- to threefold by treatment of the cells with Bay K 8644 (300 nM) and inhibited by nifedipine (4 M). In dexamethasone-treated cultures, the I–V relationship for inward current was shifted to more positive potentials in comparison with control cells. Most cells in these cultures possessed both the HVA current and also a faster inactivating, low-voltage-activated (LVA), nifedepineresistant current. These two currents could be separated both by nifedipine and by the use of steady state inactivation of the LVA current. The two components of the Ba2+ current varied widely in their relative size. The combination of LVA and HVA currents seen in dex-induced stromal cells resembles records of voltage-operated Ca2+ channels from cultures of calvarial osteoblasts. 相似文献
37.
Claudia Hey Ignaz Wessler Kurt Racké 《Naunyn-Schmiedeberg's archives of pharmacology》1995,351(6):651-659
Alveolar macrophages were obtained by broncho-alveolar lavage of isolated rat and rabbit lungs and cultured (2.5 × 106 cells/dish) for 18 h in the absence or presence of bacterial lipopolysaccharides (LPS) alone or in combination with cytokines. Thereafter, accumulation of 3H-citrulline (NO synthase activity) and 3H-ornithine (arginase activity) were determined.During incubation of rat alveolar macrophages with 3H-arginine clear amounts of 3H-citrulline and 3H-ornithine (3.8 and 4.6% of the added 3H-arginine, respectively) were formed and most of these metabolites appeared in the incubation medium (ratios extra-/intracellular of 17 and 70 for 3H-citrulline and 3H-ornithine, respectively). When rat alveolar macrophages had been cultured with LPS the formation of 3H-citrulline was increased about 30-fold and this was accompanied by a reduction in 3H-ornithine formation of about 60%. The effects of LPS were largely attenuated by dexamethasone (10 mol/1). Inhibition of NO synthase by NG-monomethyl-l,-arginine (l-NMMA, 100 mol/1) in LPS treated alveolar macrophages reduced the formation 3H-citrulline by more than 90% and restored the 3H-ornithine formation. After culturing in the presence of LPS the ratios extra/intracellular of 3H-citrulline and 3H-ornithine were markedly enhanced and this effect was not dexamethasone sensitive. During incubation of rabbit alveolar macrophages a marked formation of 3H-ornithine (about 5.3% of the added 3H-arginine), but no significant formation of 3H-citrulline could be detected. Pretreatment with LPS tended to enhance the formation of 3H-ornithine (by 50%) without effects on 3H-citrulline. Rabbit-interferon and/or tumor necrosis factor- present together with LPS during the culture period did not result in a significant 3H-citrulline formation. Under all conditions tested, culture media of rabbit alveolar macrophages did not contain significant amounts of nitrite (less than 0.5 nmol) whereas in culture media of untreated rat alveolar macrophages 22 nmol nitrite (per 18 h) were detected, and LPS induced a 3-fold nitrite accumulation, an effect prevented by dexamethasone.In conclusion, in rabbit alveolar macrophages NO synthase activity was not detectable and could also not be induced by LPS and different cytokines, whereas in rat alveolar macrophages NO synthase was readily inducible. Alveolar macrophages of both species showed marked arginase activity. After induction of marked NO synthase activity, ornithine formation was largely reduced possibly by concomitant inhibition of arginase and/or withdrawn of arginine from arginase. 相似文献
38.
为研究淋巴细胞在哮喘发病中的作用及地塞米松(Dex)、环孢菌素A(CsA)治疗哮喘的机理,用ELISA法检测哮喘患者和对照组的外周血单个核细胞(PBMC)在植物血凝素刺激下合成白细胞介素4(IL-4)、白细胞介素5(IL-5)水平,以及Dex和CsA对哮喘患者的PBMC合成IL-4、IL-5的抑制作用。结果表明,哮喘组的IL-4、IL-5水平较对照组高(P<0.05);10-6mol/L的Dex和CsA均能抑制哮喘组PBMC合成IL-4、IL-5,增大药物浓度至2×10-6、3×10-6mol/L时,CsA对IL-5合成的抑制作用逐步增强;Dex对IL-5合成的抑制作用较CsA强(P<0.05)。提示糖皮质激素和CsA抑制IL-4、IL-5的合成是其治疗哮喘的机理之一。 相似文献
39.
目的为了探讨地塞米松对实验性变态反应性神经炎(EAN)小鼠胸腺细胞的影响。方法应用原位末端标记法和电镜检测EAN小鼠胸腺细胞的凋亡。结果以上两种方法均发现地塞米松处理组胸腺细胞凋亡率明显高于自然病程组和正常对照组。结论地塞米松可明显增强EAN小鼠胸腺细胞凋亡。 相似文献
40.
目的 应用丁胺卡那霉素地塞米松(丁卡地塞)复方脂质体玻璃体内注射以延长两种药物的半衰期.方法 大白兔随机分4组,正常眼2组和眼内炎眼2组均分别注射复方脂质体和游离药物.结果 丁卡在正常眼复方脂质体的半衰期较游离药物延长1.8倍,在眼内炎眼延长3.4倍.地塞在正常眼复方脂质体半衰期较游离药物延长22.5倍,在眼内炎眼延长46.2倍.结论 丁卡地塞复方脂质体玻璃体内注射使丁卡和地塞两种药物的半衰期有明显延长. 相似文献