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121.
夏君慧  张旭  周赛君  林捷  叶好好 《浙江医学》2002,24(8):451-453,459
目的 探讨血管紧张素转换酶(ACE)基因多态性与高血压脑梗死发病的关系。方法 采用聚合酶链反应技术(PCR),对158名健康成人和50例原发性高血压、90例高血压脑梗死患者ACE基因插入/缺失(I/D)多态性进行检测,并且非条件Logistic回归筛选出与高血压脑梗死发病相关的因素。结果 DD基因型、D等位基因频率高血压脑梗死组高于正常对照组(P<0.01)和高血压组(P<0.05)。发病年龄在60岁以上者,DD基因型、D等位基因频率高血压脑梗死组高于高血压组和正常对照组(P<0.05、P<0.01);而60岁以下起病者,DD基因型、D等位基因频率高血压脑梗死组则与高血压组、正常对照组无差别(均P>0.05),而高血压组D等位基因频率高于正常对照组(P<0.05)。ACE DD基因型是高血压脑梗死独立的危险因素,发现高血压时间是高血压脑梗死的保护因素。结论 ACE DD基因型携带者发生高血压脑梗死的危险性增高,早期发现及治疗高血压对降低高血压患者脑梗死发生有意义。  相似文献   
122.
Summary Focal cerebral ischemia was induced by occlusion of the right middle cerebral artery in hypoglycemic, normoglycemic, as well as in acute and chronic diabetic rats. The brain damage was studied after 4 days. The volume of infarction was decreased in hypoglycemia (29±19 mm3 (mean±SD) versus 58±35 mm3,P<0.0046), unaltered in acute diabetes (61±45 mm3), and increased in chronic diabetes (91±22 mm3,P<0.0463). The cortex adjacent to the infarct showed selective neuronal injury affecting the cortical layers 2 and 3. The damage was enhanced by hypoglycemia and prevented in most of the diabetic animals. The findings indicate that different mechanisms cause infarction and selective neuronal injury outside infarcts, but that both are influenced by the plasma glucose concentration.  相似文献   
123.
小鼠持续性脑缺血后NMDA受体亚单位表达的变化   总被引:7,自引:1,他引:6  
目的:研究小鼠持续性脑缺血后不同脑区NMDA受体亚单位表达的变化及其与病理损伤之间的联系。方法:采用大脑中动脉阻断法制作小鼠持续性脑缺血模型,取缺血后不同时间的皮层、海马、皮层下脑组织,用免疫印迹技术测定NMDA受体亚单位ζ1和ε1及ε2蛋白的含量。同时作冰冻切片和苏木素伊红染色,计算相应脑区神经元密度。结果:NMDA受体ζ1和ε1及ε2亚单位表达的改变发生于缺血后5h内,皮层下3个亚单位表达均明显增加,海马则各亚单位表达变化不一。脑梗塞灶和相关脑区神经元密度显著减小均出现于缺血后5h,相关脑区神经元死亡严重程度依次为皮层下组织和海马CA1区及大脑颞叶皮层Ⅲ-Ⅳ层。结论:小鼠持续性脑缺血,缺血侧脑组织NMDA受体亚单位ζ1和ε1及ε2表达的变化发生在明显的病理损害之前,表达变化程度因脑区不同,与相关脑区神经元损害的程度相应。  相似文献   
124.
A phase III multicenter study was conducted in 89 patients with known intracranial vascular lesions to evaluate an extracellular gadolinium contrast agent, gadoteridol, for intracranial magnetic resonance (MR) angiography. The pre- and postcontrast MR angiograms of 82 patients were evaluated by the unblinded investigators and by two blinded readers (A and B) for visualization of lesions; arterial and venous anatomy; extent, size, and number of lesions; and disease classification. The unblinded readers indicated that lesions were visualized better on postcontrast images in the following categories: venous anatomy, 87 (81%) of 107 lesions; arterial anatomy, 43 lesions (40%); and extent or size of lesions, 38 lesions (36%). In 29 (35%) of 82 patients, the unblinded readers determined that enhanced MR angiography provided more diagnostic information than unenhanced MR angiography. The blinded readers determined that enhanced MR angiography provided more information for visualization of vascular anatomy in more than 60% of cases. The additional information provided with gadoteridol would have changed the diagnosis in nine (8%) of 107 lesions seen by the unblinded readers, 11 (12%) of 90 lesions seen by reader A, and three (3%) of 93 lesions seen by reader B. The results confirm that the use of gadoteridol improves the visualization of intracranial vascular lesions with MR angiography. The authors conclude that development of new postprocessing algorithms will improve the utility of contrast-enhanced MR angiography.  相似文献   
125.
对32例出血性梗塞研究分析,发现常出现于脑栓塞及大面积脑血栓病人。以治疗中病情突然加重或持久症状不改善为特征,动态CT检查对本病的诊断及治疗有重要意义。  相似文献   
126.
To clarify the role of serotonin in cerebral ischemia, we examined the effects of selective serotonin reuptake inhibitors, citalopram and clomipramine, on ischemic neuronal damage in the gerbil. Pretreatment with citalopram (40 mg/kg i.p.) and clomipramine (20 mg/kg i.p.) protected against neuronal destruction of hippocampal CA1 pyramidal cells following 5 min of forebrain ischemia. Furthermore, microdialysis assays showed that a striking increase in extracellular excitatory amino acid levels during ischemia was significantly inhibited by pretreatment with citalopram and clomipramine. However, citalopram (40 mg/kg i.p.) did not alter the extracellular amino acid concentrations in normal gerbils. Thus, serotonin reuptake inhibitors have a protective effect against ischemic neuronal damage. Furthermore, the present result suggests that the protective effect is mediated through prevention of the accumulation of extracellular excitatory amino acids during and after ischemia.  相似文献   
127.
Normal blood flow and velocity in the superior sagittal sinus were measured in 30 patients. A fast two-dimensional ungated phase-contrast (PC) pulse sequence was compared with a peripherally gated cine PC technique for velocity and flow quantitation. The same imaging parameters were used for both methods. Measured values for mean velocity and flow obtained with the two methods were compared by using regression analysis and t testing. For blood flow, the correlation coefficient was 0.976. For velocity measurements, r was 0.950. Mean flow was 285 mL/min ± 19 with the ungated PC method and 281 mL/min ± 19 with the cine PC method. The mean velocities measured with the two methods were 12.94 cm/sec ± 1.1 and 13.59 cm/sec ± 1.1, respectively. There was no significant difference (paired t test) between the methods for mean flow or velocity data. This was true even though flow in the superior sagittal sinus is moderately pulsatile, as shown with the cine PC technique. The ungated PC method provided these data in 13 seconds versus 3.5 minutes for the cine PC method.  相似文献   
128.
目的 研究亚硒酸钠对沙土鼠脑缺血再灌注损伤的保护作用及其机制。方法 将50只沙土鼠随机分为5组,Ⅰ组:假手术组;Ⅱ组:缺血灌注1天处死组;Ⅲ组:缺血再灌注4天处死组;Ⅳ组:硒处理、缺血再灌1天处死组;Ⅴ组:硒处理、缺血再灌注4天处死组。采用夹闭双侧颈动脉法制备沙土鼠脑缺血再灌注模型,焦油紫染色,光镜下观察各组海马CAl区神经细胞的形态变化,电镜下超微结构变化。同时测定脑组织中丙二醛(MDA)、谷胱甘肽过氧化酶(GSH-PX)、超氧化物歧化酶(SOD)的含量。结果 硒处理组沙土鼠脑缺血再灌注后,神经细胞病理形态损伤较轻,SOD、GSH-PX含量较高,MDA含量较低。结论 硒对沙土鼠脑缺血再灌注损伤具有保护作用,其机制可能和增强脑缺血再灌注早期脑组织中SOD、GSH-PX的活性,抑制氧自由基损伤,减轻脂质过氧化反应有关。  相似文献   
129.
用微量马桑内酯注入Wistar大鼠左侧前肢运动皮质,造成急性局灶型癫痫。用光镜、电镜和体视学方法研究其运动皮质第V层结构的改变。结果显示:癫痫大鼠运动皮质灶区、灶旁区的神经细胞数和胶质细胞数均分别比对照大鼠灶区和灶旁区显著减少;灶区神经毡中突触性终末数,显著减少;突触性终末的面积分数明显减少,而树突的面积分数无变化;神经胶质突起的面积分数增加。  相似文献   
130.
MRI of the brain in diabetes mellitus   总被引:15,自引:0,他引:15  
We studied the MRI appearances of the brain in 159 patients with diabetes mellitus (DM) and 2566 agematched individuals without DM (controls). The images were reviewed for cerebral infarcts, hemorrhage, atrophy and subcortical arteriosclerotic encephalopathy. Cerebral atrophy was significantly more frequent in patients with DM than in controls (P>0.005) from the sixth to the eighth decade. The frequency of atrophy was 41.2% in the 6th decade, 60.0% in the 7th and 92.3% in the 8th decade in DM, and 19.8%, 38.9% and 56.8% respectively in controls. Unexpectedly, there was no statistically significant difference in the incidences of cerebrovascular diseases at any age.  相似文献   
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