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实验性附睾淤积症引起家犬附睾起始部主细胞超微结构异常改变,但较附睾体部所见为轻;经超声波处理后(功率0.75W/cm~2,每日一次,每次8min,连续7日)则见其明显改变、或完全恢复,且未造成附睾起始部主细胞新的损伤。本实验结果在与附睾体部主细胞相应变化进行比较后,发现由于附睾淤积症对附睾管不同部位的影响是不同的,因而这种形态和功能均已不同程度改变了的附睾不同部位的主细胞对超声波作用的反应也各不相同,这除因主细胞功能状态不同外,尚与超声波声场的不均匀有关,提示探寻超声波治疗最适宜的量不仅必要,而且是有可能找到的。 相似文献
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目的:探讨超声在贲门失弛缓症诊断中的应用价值。方法:对临床拟诊为贲门失弛缓症病人首先采用超声检查,诊断贲门失弛缓症38例,同时进行了X线钡剂食管及胃肠造影,并与40例正常人进行了对照。结果:超声对贲门失弛缓症的诊断符合率为100%,失弛缓症的食管管径明显大于正常对照组(P<0.01),管壁厚度亦大于正常对照组(P<0.01)食管蠕动明显减弱,甚者消失,扩张的食管腔内见有潴留的内容物。结论:超声对贲门失弛缓症诊断具有重要的临床应用价值,可取代传统的X线钡剂造影检查。 相似文献
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cAMP对胰岛素刺激的NIH3T3细胞丝裂原激活蛋白激酶活性的抑制作用 总被引:1,自引:0,他引:1
目的 探讨cAMP-PKA信号途径对胰岛素激活的Ras-丝裂原激活蛋白激酶(MAPK)信号途径的影响。方法 以3-异丁基-1-甲基黄嘌呤(IBMX)提高细胞内环腺苷酸(cAMP)浓度,藉四唑蓝比色法(MTT法)和蛋白免疫印迹试验分别观察cAMP对胰岛素刺激的小鼠成纤维细胞(NIH3T3细胞)的生长增殖和胞内丝裂原激活蛋白激酶(MAPK)活性的影响。结果 IBMX(0.5mmol/L)抑制静息的和胰岛素(10mU/mL)刺激的NIH3T3细胞的增殖,作用呈时间依赖性。在胰岛素(10mU/mL)刺激的NIH3T3细胞,MAPK出现酪氨酸磷酸化;而以IBMX(0.5mmol/L)预处理细胞30min后,再以胰岛素作用10min,胰岛素刺激的MAPK的酪氨酸磷酸化受抑制。结论:cAMP可通过抑制MAPK磷酸化活化对NIH3T3细胞增殖起抑制作用。 相似文献
47.
肾上腺髓质素对内皮素促家兔气道平滑肌细胞增殖的抑制作用 总被引:3,自引:0,他引:3
在体外培养的家兔气道平滑肌细胞(ASMC)上,观察肾上腺髓质素(AM)对内皮素(ET)促ASMC增殖的影响及丝裂素活化蛋白激酶(MAPK)活性的变化。以探讨AM对ASMC增殖的调控。结果显示10-8mol/LET-1显著刺激ASMC3H-TdR参入及MAPK激活(P<0.01)。AM(13-52)呈剂量依赖地抑制ET-1的上述作用(P<0.05,P<0.01)。单独应用AM(13-52)对ASMC3H-TdR参入及MAPK活性无明显影响。表明AM(13-52)可抑制ASMC对ET-1的增殖反应,其机理可能涉及MAPK活性的抑制。 相似文献
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M. M. Moens A. V. Mertens L. S. De Clerck H. P. Van Bever C. H. Bridts W. J. Stevens 《Pediatric allergy and immunology》1993,4(2):89-92
In patients with allergic asthma and rhinitis high numbers of hypodense eosinophils (HE) have been demonstrated. In a previous study we reported that asthmatic and healthy children had more HE than their adult counterparts. We assumed that this might, in part, he due to the presence of immature eosinophils in children. To distinguish between immature and activated eosinophils, determination of eosinophil cationic protein (ECP) might be interesting as it is known that high serum levels of ECP are associated with increased activation of eosinophiis. In this study we determined (he levels of ECP in scrum in asthmatic and healthy children and adults trying to distinguish activated from immature eosinophils. We found that ECP levels were not increased in children (healthy and asthmatic) compared to adults (healthy and asthmatic). This supports the hypothesis that increased numbers of HE in childhood are, at least in part, immature eosinophils. Nevertheless, we could confirm that inflammation was present in children because soluble interleukin-2-receptor (slL-2R), a marker of lymphocyte activation, was higher in asthmatic children as compared to healthy children. IL-6, a marker of macrophage/monocyte activation, was not different in the different patient groups. We conclude that although signs of inflammation are present in childhood asthma, the increased numbers of HE in children are in part due to the presence of immature eosinophils. 相似文献
50.
E. Hård J. Engel Ann-Sofie Lindh 《Journal of neural transmission (Vienna, Austria : 1996)》1988,73(3):217-237
Summary The present study was undertaken to investigate the involvement of the noradrenergic neurotransmission system in the ultra sonic callings emitted by rat pups separated from their mother and exposed to cold stimulation. The investigation was primarily performed by help of agents selectively affecting the -adrenoceptors: the 2-agonist clonidine, the 1-antagonist prazosin and the 2-antagonist idazoxan.Clonidine dose-dependently stimulated the amount of ultra sonic vocalization, an effect not solely dependent upon the effect of clonidine on body temperature. In a developmental study it was found that clonidine uniformly stimulated crying at all ages from 4 days of age up to 18 days of age, that is during the whole preweaning period. Clonidine stimulated ultrasonic crying in rat pups, devoid of presynaptic catecholamine (CA) neurons by combined pretreatment with the monoamine depletor, reserpine, and the inhibitor of CAsynthesis, -methyl-tyrosine. This finding suggested that the stimulating effect of clonidine on ultrasonic vocalization was mediated by postsynaptic adrenoceptors.In pups, 12 days of age, idazoxan blocked the effect of cold stimulation on ultra sonic crying, suggesting that 2-adrenoceptors, presumably postsynaptic ones, mediated this kind of stimulation. Idazoxan also antagonized the effect of clonidine, but only at a dose effective also in control pups. Prazosin had no effect on cold-stimulated crying, but antagonized the effect of clonidine, suggesting that the effect of clonidine was also mediated by 1-receptors. At 18 days of age, prazosin no longer antagonized the effect of clonidine, whereas the antagonizing action of idazoxan was reinforced.The age-dependent variation in responsiveness to the adrenergic drugs suggest maturational changes in the function of the CA-system occurring between 12–16 days of age. 相似文献