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51.
本文在复时谱(cepstrum)分析的基础上,提出了复会动作电位传播速度的逐次提取法,指出了这个方法在实际应用中遇到的各种问题,采用指教加权和参考曲线成功地解决了这些问题。这一方法的特点是速度分辨率高,并且不要求测量点到刺激点有很大的距离。仿真实验和动物实验均表明,这一方法准确,简便,可靠。  相似文献   
52.
We describe the pattern of cognitive profiles within a community-based sample of patients with Parkinson's disease (PD) and dementia (PDD) using cluster analyses, and compare the results with data from patients with Alzheimer's disease (AD) and dementia with Lewy bodies (DLB). Fifty patients with PDD and 39 with AD from Stavanger, Norway, and 62 patients with DLB from San Diego, CA, USA were diagnosed by either standardized clinical procedures or criteria (all PDD and all AD cases) or necropsy (all DLB cases). Four subgroups were identified: two subgroups with a subcortical cognitive profile (one with mild and one with moderate dementia severity), one subgroup with global impairment and severe dementia, and one subgroup with a cortical cognitive profile and moderate dementia. Of the patients with PDD and with DLB, 56% and 55%, respectively, had a subcortical cognitive profile, compared with only 33% of the AD patients. Conversely, 30% of the patients with PDD and 26% of those with DLB had a cortical cognitive profile, compared with 67% of the patients with AD. These findings suggest that in some patients with PDD, frontosubcortical changes are the main contributing factor to dementia, whereas in other patients, cortical and hippocampal changes are more important.  相似文献   
53.
Excitatory amino acids may cause neuronal damage and death in cerebral hypoxia and ischemia, through the activation of different subtypes of glutamate receptors, in particular of the (NMDA) receptor. In the present work, the effect of hypoxia on the component of the field excitatory postsynaptic potential (fepsp) mediated by the NMDA receptor was studied in the hippocampal CA1 area of the rat. A period of 15 min of hypoxia induced virtual abolition of the NMDA receptor-mediated fepsp and a 94.8 ± 0.7% maximal decrease in the fepsp. A period of 3 min of hypoxia induced a 89.3 ± 12.3% maximal decrease in the NMDA receptor-mediated component of the fepsp and only a 50.8 ± 11.5% maximal decrease in the fepsp. Both periods of hypoxia thus induced a more pronounced depression of the NMDA receptor-mediated component of the fepsp than of the fepsp. We found that 48.5 ± 9.1% decrease (about half of the total decrease) in the NMDA receptor-mediated fepsp, and 51.6 ± 19.6% decrease (approximately all decrease) in the fepsp induced by hypoxia (3 min) were reversed in the presence of the selective adenosine A1 receptor antagonist, 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) (50 nM), and thus likely to be mediated by endogenous adenosine, through the activation of adenosine A1 receptors. On the other hand, under the conditions we assumed to be normoxic in our slices, DPCPX (50 nM) induced a much larger increase in the amplitude of the NMDA receptor-mediated fepsp compared to the increase in the fepsp, which suggest that endogenous adenosine is inhibiting predominantly the NMDA receptor-mediated fepsp under these conditions. Hypoxia markedly decreases the NMDA receptor-mediated fepsp in the hippocampal CA1 area. The contribution of endogenous adenosine to the inhibition of the NMDA receptor-mediated fepsp may be fundamental for its neuroprotective effects.  相似文献   
54.
The pathogenesis of cognitive impairment in alcoholics remains unclear. Previous studies suggested that diffuse white matter atrophy is associated with cognitive impairment in alcoholics. To elucidate this issue, the present study evaluated alcoholics with cognitive impairment using the somatosensory evoked potential (SEP) recovery method, which is suitable for detecting subtle dysfunction at the cortical level. Subjects comprised 12 alcoholics with mild cognitive impairment [Mild group: Mini Mental State Examination Score (MMSE), ≥24; mean, 27.9 ± 1.6], 12 alcoholics with moderate to severe cognitive impairment (Moderate group: MMSE score, < 24; mean, 21.0 ± 2.5) and 12 normal subjects (Control group). SEP was recorded from the hand sensory area contralateral to the median nerve stimulated at the wrist. Single-pulse or paired-pulse stimuli at various interstimulus intervals (10–300 ms) were administered. Recovery functions of N9 (a peripheral nerve component), N20, N20-P25 and P25-N33 (cortical components) were studied. N20 recovery curves of both alcoholic groups were less suppressive than those of Controls, and P25-N33 recovery curves of the Moderate group were more excitatory than those of the Mild or Control groups. A disinhibited recovery pattern of N20 indicates subcortical dysfunction, and a disinhibited pattern of P25-N33 would be induced by cortical dysfunction. Therefore, subcortical dysfunction indicated by an abnormal N20 recovery pattern may contribute to the early cognitive impairment of alcoholics, whilst the cortical dysfunction indicated by an abnormal P25-N33 recovery pattern may contribute to the later cognitive impairment of alcoholics.  相似文献   
55.
目的探讨室性早搏前后RT间期变化的规律。方法选取单发、有完全代偿间期的室性早搏心电图,测量室早及其前后相邻波群(简称室早前、室早、室早后)的RT间期,进行对比。对室早前心室舒张时间与室早RT间期变化的关系进行分析。结果RT间期由短到长的顺序为:室早<室早前<室早后。室早前心室舒张时间与室早RT间期无线性相关关系。结论室早时RT间期最短,室早后RT间期最长,这一变化规律与心室舒张时间无关。  相似文献   
56.
目的:探讨dl-3-正丁基苯酞软胶囊(恩必普软胶囊)治疗慢性脑供血不足的临床疗效及对慢性脑供血不足病人认知功能改善的影响。方法:将60例慢性脑供血不足病人随机分为治疗组和对照组,每组30例,治疗组口服dl-3-正丁基苯酞软胶囊,每次200毫克,每日3次;对照组口服复方丹参片,每次4片,每日3次,疗程为8周,治疗前后进行疗效评价和P300数据采样,同时给予同步MMSE、HDS量表评分。结果:治疗组总有效率为70%,对照组总有效率为53.3%,2组治疗后比较差异有显著意义(P<0.05);治疗组治疗前、后MMSE和HDS量表得分情况比较,均有明显改善(P<0.01),与对照组治疗后比较差异有显著意义(P<0.05);治疗组治疗前、后P300波潜伏期及P300波幅差异均有显著意义(P<0.05),与对照组治疗后比较均有显著差异(P<0.05)。结论:dl-3-正丁基苯酞软胶囊对慢性脑供血不足病人安全有效。  相似文献   
57.
The purpose of this study was to determine whether the late component of somatosensory evoked potentials (SEP) induced by electrical tooth stimulation and pain intensity are inhibited by heterotopic ischemic stimulation. The tourniquet pressure with 50 mmHg greater than the individual's systolic pressure was applied to the left upper arm for 10 min as ischemic conditioning stimulation. The late component of SEP and visual analogue scale (VAS) were recorded at 4 times and both were significantly decreased when ischemic conditioning stimulation was applied. The maximum reductions in SEP amplitude and the VAS value were 26.1% and 21.2%, respectively, during ischemic conditioning stimulation. After-effect was observed 5 min after removal of the conditioning stimulation. The present study revealed that heterotopic ischemic stimulation attenuated the late component of SEP induced by electrical tooth stimulation, triggering diffuse noxious inhibitory controls (DNIC) and after-effects in the trigeminal nerve territory. It was also suggested that the DNIC effect differs, depending on the intensity, kind, and quality of the test and conditioning stimuli.  相似文献   
58.
瞬时受体电位通道蛋白(TRP)家族由一类特殊的阳离子通道蛋白组成,在神经细胞及其他非兴奋细胞中有重要作用,其中在介导多种感觉生理功能方面的作用尤其显著.TRP结构与功能的深入研究为阐明感觉生理功能的分子机制提供了重要线索.本文综述TRP家族在温度感受、机械刺激感受、光感受和化学信号感受等方面的研究进展.  相似文献   
59.
Mirror movements (MM) occur in early, asymmetric Parkinson's disease (PD). To examine the pathophysiology of MM in PD, we studied 13 PD patients with MM (PD-MM), 7 PD patients without MM (PD-NM), and 14 normal subjects. Cross-correlogram did not detect common synaptic input to motoneuron pools innervating homologous hand muscles in PD-MM patients. Transcranial magnetic stimulation studies showed no significant difference in ipsilateral motor-evoked potentials between PD-MM patients and normal subjects. The MM side of PD-MM patients showed a slower increase in ipsilateral silent period area with higher level of muscle contraction than the non-MM side and normal subjects. There was less interhemispheric inhibition (IHI) at long interstimulus intervals of 20 to 50 ms in PD-MM than PD-NM. IHI reduced short interval intracortical inhibition in normal subjects and PD-NM, but not in PD-MM. IHI significantly increased intracortical facilitation in PD-MM and PD-NM patients, but not in normal subjects. Our results suggest that MM in PD is due to activation of the contralateral motor cortex. PD-MM patients had reduced transcallosal inhibitory effects on cortical output neurons and on intracortical inhibitory circuits compared to PD-NM patients and controls. These deficits in transcallosal inhibition may contribute to MM in PD patients.  相似文献   
60.
[目的]探讨副神经移位膈神经重建高位颈髓损伤大鼠呼吸功能后膈肌的病理学变化及膈肌运动诱发电位(motion evoked potential,MEP)的特点。[方法]健康雄性SD大鼠60只。随机分为1~6个月6个时间组。取下颈部正中切口,将双侧副神经在锁骨下水平发出内、外侧支之前切断,移位缝接膈神经干起始部。术后第1~6个月各组样本取颈后正中切口,切除C3全椎板充分显露颈髓并于C3、4水平锐性横断。证实胫前肌MEP完全消失后,于两侧腋前线肋下缘作切口,显露该处膈肌腹腔侧。直视下将同心针电极于腋前线第9肋骨下缘垂直胸壁插入膈肌肋部,监测其MEP的变化。然后完整取出膈肌,于电子天平称重。并于右侧腋前线顺膈肌肌纤维方向切取2 mm宽肌条行HE染色。分析膈肌肌纤维截面积的变化。[结果]神经移位后随着时间延长,大鼠膈肌MEP潜伏期逐渐缩短,波幅逐渐增大。6个月组MEP波幅为(6.35±0.51)mV,潜伏期为(3.41±0.36)m s。同时,膈肌逐渐饱满,肌重逐渐恢复,6个月为正常对照组的(97.23±4.07)%。肌纤维截面积也逐渐增大,6个月组达(1 741±439)μm2为正常对照组(1 809±461)μm2的(98.28±3.65)%。6个月组的各数据与对照组比无显著差异(P>0.05)。[结论]从电生理及病理学来看副神经可作为运动神经移位膈神经重建高位颈髓损伤后呼吸功能。  相似文献   
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