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1.
Objective: To study the diagnostic value of T2^*-weighted first-pass perfusion imaging in breast tumors. Methods: We analyzed the magnetic resonance imaging (MRI) information along with the pathological and immunohistochemistry results. Magnetic resonance imaging was performed in 28 patients with breast tumor. The time to signal intensity curves were generated according to the T2^*-weighted first-pass perfusion imaging. The curve's maximal signal intensity drop rate and maximal signal intensity decrease time were analyzed and compared with the pathological diagnoses after surgery. Results: Malignant breast lesions showed higher maximal signal intensity drop rate (44.69% ± 17.07 vs. 17.22% ±7.49, P 〈 0.001) than benign lesions, but there was no significant difference of maximal signal decrease time between those two lesions (23.94 s ± 4.92 vs. 20.02 s ± 6.83, P 〉 0.05). Conclusion: The T2^*-weighted first-pass perfusion imaging has enough sensitivity and specificity in breast tumor diagnosis.  相似文献   
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股骨头缺血性坏死是骨科领域尚未解决的问题之一。自1983年3月 ̄1994年1月,作者采用带旋髂深血管蒂髂骨骨膜治疗股骨头缺血性坏死60例(75侧),经过3 ̄11年随访,并采用股骨头缺血坏死疗效百分评价法判定,优良率占88.5%。其具有以下优点:(1)清除死骨彻底减压;(2)重建股骨头血液循环系统;(3)带血管的骨膜杆玫可为股骨头带入成骨效应成分,加速骨重建。此种手术方法适于治疗各种类型股骨头缺血坏  相似文献   
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为了进一步主宰骨间前神经移位术式的可行性,选用10例新鲜前臂标本,对骨间前神经旋前方肌支、鱼际肌支及尺神经深支进行显微解剖,发现正中神经旋有方肌支前径为(1.5±0.4)mm,分别测量各肌支的有骨神经纤维数为(866±144)条;正中神经鱼际返支直径为(1.7±0.3)mm,有糊神经纤维数为(1120±97);尺神经深支直径为(2.1±0.4)mm,有髓神经纤维数为(1368±120)条。用神经移  相似文献   
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1 临床资料 本组共 10例 ,均为男性 ,年龄 13~ 5 2岁。锁骨下动脉损伤 6例 ,腋动脉损伤 4例。损伤原因 :刀伤 6例 ,玻璃割伤 2例 ,车祸 2例。急诊治疗 :吻合血管 7例 ,结扎血管 2例 ,未做手术 1例。血管造影证实锁骨下动脉、腋动脉主干不通者 6例 ,其中 2例发生患肢缺血性挛缩 ,占33 3%。后期治疗 :行臂丛神经探查及神经移植术 7例 (其中 1例同时做肌腱转位术重建伸指功能 )、2例因缺血性挛缩未手术 ,1例因仅有尺神经部分损伤而未手术2 讨论 2 1 锁骨下动脉、腋动脉的侧支循环与上肢血供 本组 10例患者 ,有 6例伤段血管结扎或阻塞而…  相似文献   
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BACKGROUND: The treatment of diffuse brain injury during an acute period is focused on relieving degrees of secondary brain injury. Generation and development of pathological changes of secondary brain injury depend on signal conduction, so down-regulating over response of astrocyte through interfering a key link of signal conduction pathway may bring a new thinking for the treatment of diffuse brain injury. OBJECTIVE: To observe the effect of over activity of extracellular signal regulated kinases 1/2 (ERK1/2) signal pathway on the response of astrocyte during an acute period of diffuse brain injury. DESIGN: Completely randomized grouping and controlled animal study. SETTINGS: Department of Neurosurgery, the Third Affiliated Hospital, Nanchang University; Department of Neurosurgery, Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology. MATERIALS: A total of 158 healthy male SD rats, of 11 weeks old, weighing 320–370 g, were provided by Experimental Animal Faulty, Tongji Medical College, Huazhong University of Science and Technology. Rabbit-anti-phosphorylated ERK1/2 (pERK1/2) polyclonal antibody was provided by R&D Company; rabbit-anti-glial fibrillary acidic protein (GFAP) polyclonal antibody, SP immunohistochemical kit and horseradish peroxidase (HRP)-labeled goat-anti-rabbit IgG by Santa Cruz Company; specific inhibitor U0126 of ERK1/2 signal pathway by Alexis Company. METHODS: The experiment was carried out in the Laboratory of Neurosurgery, Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology from September 2004 to March 2006. ① Detection of pERK1/2 expression: A total of 110 rats were randomly divided into sham operation group (n =5), model group (n =35), high-dosage U0126 group (n =35) and low-dosage U0126 group (n =35). Rats in the sham operation group were only treated with incision of epicranium and fixation of backup plate, but not hit. Rats in the model group were used to establish diffuse brain injury models based on Marmarou free falling body without drug intervention. Rats in the high- and low-dosage U0126 groups were injected into caudal vein with 0.1 and 0.05 mg/kg U0126, respectively, and then, rats were hit to establish injured models. Every 5 rats were collected from model, high- and low-dosage U0126 groups at 5, 30 minutes, 3, 12, 24, 72 hours and 7 days after diffuse brain injury to detect pERK1/2 expression in cortex of parietal lobe based on Western blot technique. ② Distribution of pERK1/2 and positive GFAP cells in brain tissue: Another 48 rats were randomly divided into sham operation group (n =3), model group (n =15), high-dosage U0126 group (n =15) and low-dosage U0126 group (n =15). The intervention and administration were dealt as the same as those mentioned above. Every 3 rats were collected from model, high- and low-dosage U0126 groups at 30 minutes, 3, 12, 24 and 72 hours after model establishment to observe the distribution of pERK1/2 and postive GFAP cells in brain tissue which was cut from coronal section at Bregma –4.8 mm layer with immunohistochemical staining. MAIN OUTCOME MEASURES: pERK1/2 expression in cortex of parietal lobe and distribution of pERK1/2 and positive GFAP cells in brain tissues. RESULTS: ① pERK1/2 expression: After diffuse brain injury, pERK1/2 expression in cortex of parietal lobe was rapidly increased in the model group, reached at peak at 5 minutes and then decreased gradually. But the expression was still in a high level until the 72nd hour and fallen to the basic level on the 7th day. pERK1/2 level was lower in high- and low-dosage U0126 groups than that in model group at various time points (P < 0.01); meanwhile, pERK1/2 level was lower in high-dosage U0126 group than that in low-dosage U0126 group. The results showed that there was a certain dosage dependence on pERK1/2 expression. ② Distribution of pERK1/2 and positive GFAP cells in brain tissue: Positive expression of pERK1/2 lasted in brain tissue from 30 minutes to 72 hours after diffuse brain injury (P < 0.05). In addition, from 30 minutes to 3 hours, brown-yellow stained cells were mainly distributed in plasma, but rarely in nucleus. A lot of positive cells had tree-like apophysis, which was similar to neurons. With the time passing by, more and more nuclei manifested positive stains; moreover, nuclei mainly manifested positive staining until 24 hours after diffuse brain injury. Immune-positive pERK1/2 cells were widely distributed in brain tissue, especially mainly in binding site between deep cortex and cerebral white matter, and then in hippocampus. In addition, ependymal cell and vascular endothelial cells of choroids plexus also manifested strongly positive staining. As compared with model group, positive cells were decreased gradually in high- and low-dosage U0126 groups. However, number of positive cells was less in high-dosage U0126 group than that in low-dosage U0126 group. CONCLUSION: Diffuse brain injury strongly induces the activity of ERK1/2 signal pathway and response of astrocyte; in addition, U0126 can inhibit response of glial cells during an acute period, and the effect manifests dosage dependence.  相似文献   
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全国骨坏死研讨会纪要   总被引:2,自引:0,他引:2  
由《骨与关节损伤杂志》编辑部、全军显微外科专业组及《中华医学杂志》编辑部主办的第1次全国骨坏死研讨会于1993年11月2~4日在桂林召开。来自24个省市自治区和部队的77名代表出席了会议,收到论文81篇,代表们对如下6个专题进行了讨论。  相似文献   
8.
Objective: To establish a prostatic hyperplasia model with beagle dogs. Methods: Twenty-four male beagle dogs, 2 years of age, were divided into the treatment and control groups at random and were administrated testosterone propionate (TP) i.m. two months after castration. Three treatment groups were set with the doses of TP at 0.8 mg/kg, 2.5 mg/kg and 7.5 mg/kg, respectively, and the control was given the same volume of vehicle. Two months later, half of the animals were killed and sera samples were obtained. The wet weight and volume of prostate were measured. The dihydro testosterone (DHT) level of the serum and prostate were determined with the commercial radioimmunoassay (RIA) kit. The prostate was sectioned, fixed and stained with hematoxylin and eosin. Pictures were taken with a digital camera under the microscope and were analyzed with a computer for the epithelial cell height and the acinar luminal area with micro image analysis software. The prostate volume was measured with ultrasonic diagnost  相似文献   
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AnAnalysisofChromosomeonSterilityCausedbyAzoospermiaorOligospermia¥WuMeiheng;TangWingnuo.(ACTAACADEMIAEMEDICINAENANJING,1995(...  相似文献   
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