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31.
我院骨科组于1985年5~10月份为4例患下肢高分化低度恶性肿瘤的病人,在化疗的配合下施行肿瘤局部大块切除,吻合血管的背阔肌肌皮瓣移植修复创面等综合治疗,早期获得了满意的效果.4例病人中有2例患小腿软骨肉瘤,1例小腿脂肪肉瘤和1例髋部纤维肉瘤.背阔肌肌皮瓣较适用于修复软组织缺损大的创面,其大而扁平的肌肉部分几乎能完全覆盖缺损,外形亦常较满意.  相似文献   
32.
在53只乌拉坦麻醉家兔身上,观察到延髓孤束核(NTS)区注射γ-氨基丁酸(GABA)使血压显著下降,安定(DZ)有相似的降压效应,荷包牡丹碱(BIC)和印防己毒素(PIC)则使血压升高;促甲状腺素释放激素(TRH)和甲硫脑啡肽(MTP)对血压无明显影响;延髓的另一些区域应用GABA等药物后血压变化不明显;提示GABA能神经递质系统参与心血管活动的抑制性中枢调节,NTS区是其作用部位之一。  相似文献   
33.
The changes in spike activity of single neurons of the compact part of the substantia nigra, evoked by nucleus caudatus stimulation under conditions of long-term registration of the single and multiple, isolated and combined actions of GABA, GABA-amide, glutamine, and ethanolamine-O-sulfate (EOS) were studied in albino rats. Inhibition of poststimulus activity under GABA action was recorded and the inhibitory effect of GABA-amide was revealed. Primary excitatory and subsequent inhibitory effects of glutamine in combination with EOS were shown. The subsequent administration of bacterial melanin, synthesized by a mutant culture of Bacillus thuringiensis (BT-M) evoked a clear-cut and prolonged excitatory reaction during all the combined actions of GABA, GABA-amide, glutamine, and EOS. Preliminary administration of BT-M abolished the inhibitory poststimulus effects of GABA, GABA-amide, and EOS, as well as glutamine-induced excitation.  相似文献   
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The medial globus pallidus plays a crucial role in generation of L‐DOPA‐induced dyskinesia in patients with Parkinson's disease. The 6‐hydroxydopamine‐lesioned rat exhibiting behavioral sensitization to L‐DOPA is one useful animal model for examining L‐DOPA‐induced dyskinesia. To determine neuropathological abnormality responsible for behavioral sensitization, the medial globus pallidus and the substantia nigra reticulata in 6‐hydroxydopamine‐lesioned rats treated with L‐DOPA were examined. Intermittent L‐DOPA treatment induced hypertrophy of the lesioned‐side of medial globus pallidus and substantia nigra reticulata of 6‐hydroxydopamine‐lesioned rats with behavioral sensitization to L‐DOPA. Additionally, coadministration of a 5‐HT1A receptor agonist, 8‐hydroxy‐2(di‐n‐propylamino)tetralin with L‐DOPA, alleviated the hypertrophy with improvement of the behavioral sensitization. These results suggest that hypertrophy of the medial globus pallidus and substantia nigra reticulata is associated with induction of behavioral sensitization to L‐DOPA in 6‐hydroxydopamine‐lesioned rats. Therefore, neuropathological changes corresponding to hypertrophy might underlie L‐DOPA‐induced dyskinesia in patients with Parkinson's disease.  相似文献   
36.
目的 比较大脑皮质向脊髓与红核发出投射的区域并探讨是否有分支投射存在。方法 将。TB及NY分别注入大白鼠的脊髓与红核内,在大脑皮质观察比较标记细胞出现的部位。结果 FB标记细胞出现在24,10,8,6,4,3,1,2,23,29b,29c,18,7,13,39区。NY标记细胞出现于6,4,3,1区,10区的尾侧部及7,18区的颅饲部亦有少量存在。无发现双标记细胞。结论 大脑皮质向脊髓发出投射的区域非常广泛,向红核发出投射的区域全部重叠于皮质脊髓神经元分布的区域内,皮质脊髓神经元无分支投射到红核。  相似文献   
37.
Profound reductions in cortical acetylcholine levels together with degeneration of cholinergic neurons in the basal forebrain have been reported in patients with Alzheimer's disease. A similar loss of the cholinergic neurons of the basal forebrain and impairment of learning and memory occur in animals injected with a nerve growth factor-diphtheria toxin conjugate, suggesting that this animal model is suitable to analyze cholinergic roles on learning and memory processes, and also the pathogenesis of Alzheimer's disease. In addition, animal models constructed by electrolytic or neurotoxic lesioning of the basal magnocellular nucleus, and models made by transgenetic technology were described.  相似文献   
38.
实验性大鼠大脑皮层梗死后继发丘脑损害与DNA氧化损伤   总被引:1,自引:1,他引:0  
目的观察大鼠大脑皮层梗死后丘脑腹后外侧核(ventroposterior nucleus of the thalamus,VPN)的继发性损害是否有DNA氧化损伤,并研究抗氧化剂依布硒啉(ebselen,EB)对这种远隔部位损伤是否具有改善作用。方法采用易卒中型肾血管性高血压大鼠(stroke-prone renovascular hypertensive rats,RHRSP),建立大脑中动脉皮层支闭塞(middle cerebral artery occlusion,MCAO)模型后分为:①假手术组,②模型组,③溶剂组,④抗氧化剂EB10mg.kg-1组,⑤抗氧化剂EB30mg.kg-1组,每组5只大鼠。2周后行肢体运动神经功能评估并取VPN后行尼氏染色,免疫组化检测VPN的8-羟基-2-脱氧马苷(8-hydroxy-2-deoxyguanosine,8-ohdG)表达。结果EB10mg.kg-1组和EB30mg.kg-1组神经功能评分优于假手术组(1.80±0.56,1.72±0.48vs2.28±0.33,P<0.05)。尼氏染色可见假手术组同侧VPN细胞形态规整。而梗死同侧VPN神经细胞出现细胞体积变小,胞核固缩,尼氏体退变为萎缩的深色细胞。EB30mg.kg-1组尼氏染色观察到改善作用。溶剂组同侧VPN的8-ohdG阳性细胞数目(0.1mm2)显著增加(146.8±12.1vs108.4±19.2,P<0.05);与溶剂组相比,EB10mg.kg-1组和EB30mg.kg-1组阳性细胞数目显著下降(123.6±14.7,123.4±17.4vs146.8±12.1,P<0.05)。结论实验性大脑皮层梗死后2周,同侧VPN存在DNA氧化性损伤。抗氧化剂EB对VPN的DNA氧化损伤有抑制作用,并可改善神经功能。  相似文献   
39.
目的探讨外周高渗刺激激活下丘脑室旁核(PVN)神经元的细胞类别。方法以腹腔注射高渗盐水作为外周高渗刺激。细胞外记录PVN神经元单位放电的变化,并用免疫细胞化学方法观察PVN中los的表达及los表达阳性神经元的性质。结果腹腔注射高渗盐水使PVN的位相型放电神经元兴奋,PVN内los表达明显增加,特别是PVN大细胞中大量的los阳性神经元同时表达精氨酸加压索(AVP)。结论外周高渗刺激能够激活PVN内的加压索(VP)能神经元。  相似文献   
40.
We attempted to find out the role of α2-adrenoceptors of the medullary lateral reticular nucleus (LRN) in antinociception in rats. Spinal antinociception was evaluated using the tail-flick test, and supraspinal antinociception using the hotplate test. Antinociceptive effects were determined following local electric stimulation of the LRN, and following microinjections of medetomidine (an α2-adrenoceptor agonist; 1–10 μg), atipamezole (an α2-adrenoceptor antagonist; 20 μg) or lidocaine (4%) into the LRN. The experiments were performed using intact and spinalized Hannover-Wistar rats with a unilateral chronic guide cannula. Electric stimulation of the LRN as well as of the periaqueductal gray produced a significant spinal antinociceptive effect in intact rats. Medetomidine (1–10 μg), when microinjected into the LRN, produced no significant antinociceptive effect in the tail-flick test in intact rats. However, following spinalization, medetomidine in the LRN (10 μg) produced a significant atipamezole-reversible antinociceptive effect in the tail-flick test in the hot-plate test, medetomidine (10 μg) in the LRN produced a significant atipamezole-reversible increase of the paw-lick latency in intact rats. Microinjection of atipamezole (20 μg) or lidocaine alone into the LRN produced no significant effects in the tail-flick test. The results are in line with the previous evidence indicating brat the LRN and the adjacent ventrolateral medulla is involved in descending inhibition of spinal nocifensive responses. However, α2-adrenoceptors in the LRN do not mediate spinal antinociception but, on the contrary, their activation counteracts antinociception at the spinal cord level. The spinal aninociceptive effect of supraspinally administered medetomidine in spinalized rats can be explained by a spread of the drug (e.g., via circulation) which then directly activates α2-adrenoceptors at the spinal cord level.  相似文献   
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