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Abstract

To investigate regional differences in spontaneously released endothelium-derived relaxing factor (EDRF), a bioassay of spontaneously released EDRF was performed on rabbit basilar, ear; common carotid and thoracic arteries using an isometric tension measurement technique and a measurement of cyclic guanosine monophosphate (cCMP) content in the vascular smooth muscle. The amount of spontaneously released EDRF was higher in the basilar artery than in any other arteries examined (p < 0.01). The levels of cCMP were 57.3 ± 4.4 (n = 7) in basilar, 26.5±4.3 (n = 6) in ear; 24.5±2.3 (n = 11) in common carotidand 30.3 ±3.8 pmol/g tissue (n = 8) in thoracic artery with endothelium, while endothelium-denuded arteries showed 24.2 ± 6.6 (n = 5), 17.5 ± 5.1 (n = 6), 20.1 ± 2.9 (n = 7) and 14.4 ± 2.3 pmol/g tissue (n = 8) in the same order. Haemoglobin (10~5 m, incubated with the artery for 5 min, significantly reduced the level of cGMP in all vessels with endothelium: 35.3±4.4 (basilar), 76.0 + 2.7 (ear), 14.0±1.9 (common carotid) and 8.7 ±1.2 pmol/g tissue (thoracic artery). Since endothelium-dependent relaxation is associated with a rise in the cGMP content of the smooth muscle cell, the data of cGMP measurement in addition to the bioassay of spontaneously released EDRF in tension measurement suggests that the spontaneous release of EDRF is much greater in the basilar artery than in extracerebral arteries. It is concluded that the intensity of the spontaneously released EDRF is relatively higher in the intracerebral artery than in the extracerebral artery. [Neurol Res 1993; 15: 327-332]  相似文献   
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Abstract

The authors report the case of a patient who presented a ruptured aneurysm of the anterior communicating artery and an unruptured aneurysm of the middle cerebral artery arising at the site of a fenestration of the MCA. The fenestration was undiagnosed on the preoperative angiogram but discovered during the surgery carried out for clipping of the aneurysms. In the literature, cases of fenestration of the MCA are sporadically reported and are incidental findings; an aneurysm may be associated on an artery other than the fenestrated MCA; an aneurysm arising at the site of the MCA fenestration is a very rare occurrence.  相似文献   
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Abstract

Despite the voluminous current literature the potential of nimodipine to modify the outcome in experimental cerebral ischaemia remains a controversial matter. The authors have evaluated in controlled double blind experiments the influence of a continuous i.v. infusion of the drug (1 ¼g kg-1 min-1) upon infarct size, histopathology and neurological outcome in rats with permanent middle cerebral artery (MCA) occlusion. The infusion was started 20 min before induction of ischaemia and continued 4 hours thereafter. The nimodipine treated animals were subdivided into hypotensive (MABP lower than 85 mmHg for more than 5 min after arterial occlusion) and normotensive groups. Infarction size, documented by TTC, H&E and Nissl staining was significantly smaller (p < 0.001) in nimodipine normotonic rats than the lesions in placebo and saline treated ratsas well compared with hypotonic nimodipine animals (largest infarction). These differences were found to be entirely at the expense of the cortical (frontoparietal) component of the lesion, suggesting ‘penumbra’ action of the drug. Moreover, nimodipine normotonic rats displayed lower cortical neuronal injury in the periinfarct zone. These findings were corroborated by corresponding better neurological scores. Our results indicate that nimodipine is effective in reducing focal cerebral ischaemia, provided the MABP is maintained higher than 85 mmHg.  相似文献   
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Abstract

The haemodynamic mechanisms responsible for the appearance of paraparetic transient ischaemic attacks in ten patients with childhood moyamoya disease who subsequently underwent bifrontal omental transplantation were investigated. Cerebral perfusion (CP) was measured with 99mTc-hexamethylene-propyleneamine oxime single photon computed tomography prior to and after administration of acetazolamide. Cerebral perfusion was obtained by dividing radioisotope uptake per pixel in regions of interest by that in cerebellum. Haemodynamic reserve was defined as [CP after acetazolamide - CP before acetazolamide]/CP before acetazolamide × 100. Amounts of CP in the anterior portion of the frontal lobe and in the paracentral lobule were 0.70±0.04 and 0.74 ±0.03, respectively, before appearance of the transient ischaemic attacks. The latter was significantly higher than the former (p <0.0001). Haemodynamic reserves were -11.1 ±2.8 and - 9.6 ± 3.0, respectively, at that time. These two parameters were significantly decreased just after paraparetic transient ischaemic attacks and two parameters in the paracentral lobule were more decreased than those in the anterior portion of the frontal lobe. But these increased again after bifrontal omental transplantation in these two regions. In summary, the watershed region was located anterior to the paracentral lobule before appearance of the transient ischaemic attacks, and widened and moved backward to include the paracentral lobule just before their appearance. [Neurol Res 1995; 17: 162-168]  相似文献   
6.
The changes in endogenous amino acids in brain extracellular and intracellular compartments evoked by hyposmotic stress and energy deprivation were compared. Tissue content and release of ten amino acids were measured simultaneously in rat hippocampal slices by means of high performance liquid chromatography Hyposmotic stress induced a large release of taurine (25568 pmol mg-7 protein), and a smaller release of glutamate, accompanied by an inverse change in tissue content. Adding mannitol to correct osmolarity blocked these changes. Energy deprivation caused an increase in the release of all amino acids except glutamine. The release was particularly large for glutamate and GABA (31141 and 13282 pmol mg–1 respectively). The intracellular concentrations were generally reduced, but the total amount of the released amino acids increased. In contrast to the effect seen during hyposmolar stress, mannitol enhanced the changes due to energy deprivation. The results show that hyposmolar stress and energy deprivation cause different content and release profiles, suggesting that the mechanisms involved in the two situations are either different, or modulated in different ways. The intracellular amino acid depletion seen during energy deprivation shows that increased outward transport is probably a primary eventL, and increased amino acid formation likely secondary to this release. [Neurol Res 1995; 17: 402–408]  相似文献   
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Physical exercise preconditioning is known to ameliorate stroke‐induced injury. In addition to several other mechanisms, the beneficial effect of preischemic exercise following stroke is due to an upregulated capacity to maintain energy supplies. Adult male Sprague‐Dawley rats were used in exercise and control groups. After 1–3 weeks of exercise, several enzymes were analyzed as a gauge of the direct effect of physical exercise on cerebral metabolism. As a measure of metabolic capacity, an ADP/ATP ratio was obtained. Glucose transporters (GLUT1 and GLUT3) were monitored to assess glucose influx, and phosphofructokinase (PFK) was measured to determine the rate of glycolysis. Hypoxia‐induced factor‐1α (HIF‐1α) and 5′AMP‐activated protein kinase (AMPK) levels were also determined. These same analyses were performed on preconditioned and control rats following an ischemic/reperfusion (I/R) insult. Our results show that GLUT1, GLUT3, PFK, AMPK, and HIF‐1α were all increased following 3 weeks of exercise training. In addition, the ADP/ATP ratio was chronically elevated during these 3 weeks. After I/R injury, HIF‐1α and AMPK were significantly higher in exercised rats. The ADP/ATP ratio was reduced in preconditioned rats in the acute phase after stroke, suggesting a lower level of metabolic disorder. GLUT1 and GLUT3 were also increased in the acute phase in exercise rats, indicating that these rats were better able to increase rates of metabolism immediately after ischemic injury. In addition, PFK expression was increased in exercise rats showing an enhanced glycolysis resulting from exercise preconditioning. Altogether, exercise preconditioning increased the rates of glucose metabolism, allowing a more rapid and more substantial increase in ATP production following stroke. © 2013 Wiley Periodicals, Inc.  相似文献   
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