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101.
目的:探讨一氧化氮(NO)与先天性心脏病(CHD)引起的肺动脉高压(PH)发病间的关系。方法:应用NO试剂盒检测了CHD患儿肺动脉及上腔静脉血浆中NO含量。结果;(1)伴PH组肺动脉血浆NO含量明显高于不伴肺动脉高压组(37.58±9.99μmol/L:19.03±15.25μmol/L,P<0.01);(2)在PH组中,肺动脉血浆NO含量明显高于上腔静脉血(P<0.01);而不伴PH组,肺动脉和上腔静脉血浆NO含量无显著性差异(P>0.05)。结论:(1)伴PH的先心患儿肺动脉血浆NO含量升高;(2)NO可能介入了CHD引起的PH发病过程。  相似文献   
102.
目的探讨脂多糖和同型半胱氨酸是否诱导培养的人脐静脉内皮细胞表达单核细胞趋化蛋白1(MCP-1) mRNA及其机制.方法将生长至汇合的人脐静脉内皮细胞分为对照组、脂多糖组,脂多糖+SB203580组,同型半胱氨酸组,同型半胱氨酸+SB203580组,脂多糖+同型半胱氨酸组.采用斑点杂交和RT-PCR检测其MCP-1 mRNA的表达.用免疫细胞化学法检测对照组、脂多糖组和同型半胱氨酸组P38蛋白激酶蛋白的表达.结果培养的人脐静脉内皮细胞能表达较低水平的MCP-1 mRNA.斑点杂交和RT-PCR均显示各实验组的MCP-1 mRNA明显高于对照组.免疫细胞化学显示,P38蛋白激酶蛋白在对照组的细胞核阳性表达率为9.6%,当人脐静脉内皮细胞暴露于脂多糖或同型半胱氨酸后,细胞核阳性表达率升至46.7%或57.7%.结论脂多糖和同型半胱氨酸能诱导人脐静脉内皮细胞表达单核细胞趋化蛋白1 mRNA,P38蛋白激酶可能参与了该过程.  相似文献   
103.
Background: Because of the potential toxicity of nitric oxide (NO) and its oxidising product nitrogen dioxide (NO2), any system for the delivery of inhaled NO must aim at stable and predictable levels of NO and as low concentrations as possible of NO2.
Methods: In a laboratory set-up, we have evaluated mixing conditions in a system where NO is added after the ventilator with continuous flow. Mixing was studied by using carbon dioxide (CO2) as a tracer gas since capnography has a short response time (360 ms) in comparison with measurements of NO with electrochemical fuel cells (response time of 18s). CO2 (in volumes corresponding to an ideal mixture of 1,3 and 6%) was fed, after the ventilator, either into plain breathing tubing, into one or two soda lime absorbers, or into an empty and a soda lime-filled canister, at different ventilatory rates and different I: E ratios. Samples were drawn from the inspiratory limb close to the Y-piece. NO was added in the same way and in the same volume as the highest concentration of CO2.
Results: CO2 added to plain tubing resulted in peak levels up to five times the set levels, while addition to a mixing box with an empty and a soda lime-filled canister resulted in even mixing with gas concentrations close to the ideal. When NO was fed into plain tubing, low levels were measured at the Y-piece, indicating poor mixing. Gas supply to a mixing chamber resulted in even concentrations.
Conclusions: Even and predictable levels of NO can be obtained with continuous flow of NO to the inspiratory limb, after the ventilator, if a mixing chamber is used. To obtain adequate mixing, the volume of the mixing box should be greater than the tidal volume.  相似文献   
104.
目的:观察吸入一氧化氮(NO)对心瓣膜置换术后肺动脉高压患者血流动力学的影响。方法:选择9例心瓣膜置换术后伴肺动脉高压的病人,吸入NO0.003%,观察三个时象点:吸入NO前;开始吸入NO后15分钟;停止吸入NO后15分钟。结果:吸入NO能显著降低肺动脉压和肺循环阻力指数(P<0.01),停止吸入NO15分钟后,肺动脉压和肺循环阻力指数恢复到原有水平。在整个观察过程中,心率、平均动脉压、中心静脉压、肺动脉楔压、体循环阻力指数和心脏指数均无显著变化(P>0.05)。结论:吸入NO具有选择性肺血管扩张作用,是治疗心瓣膜置换术后肺动脉高压的较理想药物。  相似文献   
105.
The nitric oxide synthase (NOS) gene is thought to be associated with essential hypertension (EH), because NO is implicated in endothelium-mediated vasodilation. We investigated the possible association between the alleles of simple tandem repeat DNA polymorphism of the endothelial constitutive NOS (cNOS) gene and EH in Japanese subjects. In all, 100 patients with EH and 123 subjects with normal blood pressure were studied. Polymerase chain reaction was used to amplify the CA repeat site in the endothelial cNOS gene and alleles based on the CA repeat number were determined. The allele frequencies in the hypertensive group and normotensive group were then compared. Twenty-three alleles were identified in this study of Japanese subjects. The overall distributions of allele frequencies in the two groups were not significantly different. However, comparing the allele frequencies in the EH group without left ventricular hypertrophy (LVH) and the normotensive group, the overall distributions were significantly different (p = 0.019). The 33-repeat allele was found more frequently in the EH group without LVH than in the normotensive group (p = 0.000047, Odds ratio = 3.71). In conclusion, the 33-repeat allele of the endothelial cNOS gene is associated with EH without LVH, and may be a genetic marker of EH in Japanese subjects.  相似文献   
106.
我们对50例子宫、卵巢手术病人,使用利多卡因做硬膜外麻醉,其中25例向硬膜外腔内注入异氟醚-氧化亚氮气体。2组对比发现,实验组麻醉平面明显高于对照组,在同样手术时间内实验组所使用的利多卡因量明显少于对照组。表明异氟醚-氧化亚氮气体有增强利多卡因的硬膜外麻醉作用,同时未发现注入吸入麻醉药产生副作用。  相似文献   
107.
目的 :观察ZMW型环氧乙烷灭菌箱对异体骨材料灭菌效果 ,旨在寻找一种安全、经济的灭菌方法。方法 :清洁条件下取骨 ,制成 0 .5cm× 0 .5cm× 2cm湿润骨材料和干燥骨材料 ,抽取样本 ,用ZMW型环氧乙烷灭菌箱 (15 0L)在不同温度及时间下消毒 ,以环氧乙烷指示胶带是否变色作为灭菌指标 ,样本在消毒前后分别作细菌培养。结果 :不同消毒条件下 ,每批样本均有细菌生长 ,干燥骨材料有菌率高于湿润的骨材料。结论 :ZMW型环氧乙烷灭菌箱不能使异体骨移植材料完全达到灭菌的要求 ,环氧乙烷指示胶带不能作为骨移植材料的灭菌指标 ,干燥可能使细菌的抗环氧乙烷能力增加 ,从而间接的影响了环氧乙烷的消毒效果。  相似文献   
108.
BACKGROUND: Carbon monoxide (CO) has emerged as an endogenously produced gaseous mediator known to be involved in bronchial smooth muscle regulation. Increased amounts of CO have been found in exhaled air during asthma and lower airway inflammation. Recently CO has been shown to be produced in the nasal airways, but there are no reports of altered CO levels in nasal airways during inflammation. OBJECTIVE: This study was designed to investigate if CO levels increase in the human nasal airways during inflammatory conditions, such as allergy and upper airway respiratory tract infection (URTI). METHODS: CO was sampled separately from the upper and lower airways of 13 healthy control subjects, six patients with a history of allergic rhinitis and six patients with URTI. RESULTS: Nasal CO levels were increased in subjects with allergic rhinitis, compared to healthy controls (2.07 +/- 0.15 ppm, n = 6 and 1.62 +/- 0.08 ppm, n = 13, respectively, P < 0.01). CO levels were also increased in patients with URTI, compared to the same controls (1.92 +/- 0.09 ppm, n = 6, P < 0.05). Normal levels of CO were found in air from the lower airways among subjects with allergic rhinitis, whereas corresponding levels in the URTI patients were increased. CONCLUSION: The present data demonstrates that upper airway CO levels increase in parallel with different inflammatory stimuli, such as allergy and infection, suggesting a role for CO as marker or mediator of nasal inflammation.  相似文献   
109.
目的 :观察 3 ,6 (二甲氨基 ) 二苯骈碘杂六环葡萄糖酸盐对AGEP引起的大鼠主动脉平滑肌细胞增殖及牛主动脉内皮细胞内皮素和一氧化氮改变的影响。方法 :采用牛血清白蛋白 (BSA)与不同浓度葡萄糖 (0 ,2 0 ,5 0 ,80mmol·L-1)体外孵育制备糖基化终产物 (AGEP) ,应用 [3 H] TdR掺入法和MTT比色法观察I-93对重度糖化的AGEP诱导的大鼠主动脉平滑肌细胞 (ASMC)增殖的影响 ;应用放射免疫技术及Greiss法观察I -93对AGEP引起的牛主动脉内皮细胞 (BAEC)释放内皮素 1(ET 1)和一氧化氮 (NO)的影响。结果 :I-93 10 -7~ 10 -5mol·L-1能明显抑制AGEP引起的ASMC增殖 ,其 [3 H] TdR掺入量和MTT比色法的最大抑制率分别为79 .4%和 44 .2 %。随AGEP糖浓度的增加 (2 0~ 80mmol·L-1) ,BAEC培养液中ET 1含量亦逐渐上升 [(4 93± 63 )~ (779± 10 5 )ng·L-1] ,I -93 10 -7~ 10 -5mol·L-1能明显抑制重度糖化的AGEP促进ET 1释放的作用 ;I -93对AGEP灭活NO的作用有剂量依赖性抑制效应。结论 :I -93有抑制ASMC增殖的作用 ;对AGEP诱导的BAEC释放ET 1和NO间平衡失调有调节作用 ,在防治阻塞性血管疾病方面I -93具有潜在的应用价值  相似文献   
110.
Dystonia is a common movement disorder which is thought to represent a disease of the basal ganglia. However, the pathogenesis of the idiopathic dystonias, i.e. the neuroanatomic and neurochemical basis, is still a mystery. Research in dystonia is complicated by the existence of various phenotypic and genotypic subtypes of idiopathic dystonia, probably related to heterogeneous dysfunctions.In neurological diseases in which no obvious neuronal degeneration can be found, such as in idiopathic dystonia, the identification of a primary defect is difficult, because of the large number of chemically distinct, but functionally interrelated, neurotransmitter systems in the brain.The variable response to pharmacological agents in patients with idiopathic dystonia supports the notion that the underlying biochemical dysfunctions vary in the subtypes of idiopathic dystonia. Hence, in basic research it is important to clearly define the involved type of dystonia.Animal models of dystonias were described as limited. However, over the last years, there has been considerable progress in the evaluation of animal models for different types of dystonia.Apart from animal models of symptomatic dystonia, genetic animal models with inherited dystonia which occurs in the absence of pathomorphological alterations in brain and spinal cord are described.This review will focus mainly on genetic animal models of different idiopathic dystonias and pathophysiological findings. In particular, in the case of the mutant dystonic (dt) rat, a model of generalized dystonia, and in the case of the genetically dystonic hamster (dtsz), a model of paroxysmal dystonic choreoathetosis has been used, as these show great promise in contributing to the identification of underlying mechanisms in idiopathic dystonias, although even a proper animal model will probably never be equivalent to a human disease.Several pathophysiological findings from animal models are in line with clinical observations in dystonic patients, indicating abnormalities not only in the basal ganglia and thalamic nuclei, but also in the cerebellum and brainstem. Through clinical studies and neurochemical data several similarities were found in the genetic animal models, although the current data indicates different defects in dystonic animals which is consistent with the notion that dystonia is a heterogenous disorder.Different supraspinal dysfunctions appear to lead to manifestation of dystonic movements and postures. In addition to increasing our understanding of the pathophysiology of idiopathic dystonia, animal models may help to improve therapeutic strategies for this movement disorder.  相似文献   
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