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1.
Though cerebrovascular complications of pregnancy remain relatively rare, they represent a potentially devastating event that necessitates prompt identification and treatment. Eighteen percent of strokes occurring in young women are linked to pregnancy. They occur mostly in the third trimester or during the post-partum period. Their biggest risk factors are hypertension, preeclampsia/eclampsia and migraine. Cerebrovascular events occurring during this period may involve specific pathophysiological processes that include embolic phenomena or endothelial dysfunction, but can also have common etiologies that are simply favored by the context of pregnancy. Thus, posterior encephalopathy and vasoconstriction cerebral syndrome are relatively frequently involved in cerebrovascular complications of pregnancy. Other very specific causes like amniotic fluid embolism or postpartum cardiomyopathy can also be responsible for such events. The management of stroke during pregnancy must be multidisciplinary and include a neurovascular expertise. Some conditions can lead to a long-life follow-up and modify the management of a future pregnancy.  相似文献   
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PurposeThoracic aortic aneurysm (TAA) is a cardiovascular disease characterized by increased aortic diameter, treated with surgery and endovascular therapy in order to avoid aortic dissection or rupture. The mechanism of TAA formation has not been thoroughly studied and many factors have been proposed to drive its progression; however strong focus is attributed to modification of smooth muscle cells (SMCs). Latest research indicates, that microRNAs (miRNAs) may play a significant role in TAA development – these are multifunctional molecules consisting of 19–24 nucleotides involved in regulation of the gene expression level related to many biological processes, i.e. cardiovascular disease pathophysiology, immunity or inflammation.Materials and methodsPrimary SMCs were isolated from aortic scraps of TAA patients and age- and sex-matched healthy controls. Purity of isolated SMCs was determined by flow cytometry using specific markers: α-SMA, CALP, MHC and VIM. Real-time polymerase chain reaction (RT-PCR) was conducted for miRNA analysis.ResultsWe established an isolation protocol and investigated the miRNA expression level in SMCs isolated from aneurysmal and non-aneurysmal aortic samples. We identified that let-7 g (0.71-fold, p = 0.01), miR-130a (0.40-fold, p = 0.04), and miR-221 (0.49-fold, p = 0.05) significantly differed between TAA patients and healthy controls.ConclusionsFurther studies are required to improve our understanding of the pathophysiology underlying TAA, which may aid the development of novel, targeted therapies. The pivotal role of miRNAs in the cardiovascular system provides a new perspective on the pathophysiology of thoracic aortic aneurysms.  相似文献   
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目的探讨浅表食管癌侵袭深度及分化程度与区域淋巴结转移的关系。方法本院2002年6月至2004年6月总共手术治疗食管癌923例,其中早期浅表食管癌68例,本文就对其术后侵袭深度及分化程度与区域淋巴结转移情况进行回顾性分析。结果本组无手术死亡,全组淋巴结转移率27%,其中高出黏膜型食管癌的淋巴结转移率为38%,侵袭越深,淋巴结转移率越高;分化程度越低淋巴结转移率越高。结论高度重视浅表型食管癌的根治性,对早期食管癌也应按肿瘤外科的原则行食管的次全切除术并常规清扫区域淋巴结。  相似文献   
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目的:观察抗人VEGF单抗E11对小鼠肉瘤S180生长的影响。方法:BALB/c小鼠45只,接种小鼠肉瘤细胞株S180,随机均分为5组。其中3组于接种后1—4、7—11天,分别通过腹腔或瘤周皮下注射抗人VEGF单抗E11100μg、200μg。另以生理盐水及5—Fu注射作阴性及阳性对照组。接种后第14天处死小鼠并称取瘤重,计算抑瘤率,并做组织病理学检查。结果:抗人VEGF单抗皮下及腹腔给药均可抑制S180肉瘤的生长,且抗人VEGF单抗200μg/d组抑瘤率均高于5—Fu组;皮下给药组抑瘤率最高,达67.2%。结论:不同剂量、不同给药途径的抗人VEGF单抗对小鼠肉瘤S180的生长均有明显抑制作用,说明抗人VEGF单抗可通过阻断VEGF的作用,抑制肿瘤血管生成,从而达到抑制肿瘤生长的目的。提示抗人VEGF单抗具有可能的临床应用前景。  相似文献   
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降钙素基因相关肽对人牙髓细胞的矿化影响   总被引:2,自引:2,他引:2  
目的:分析降钙素基因相关肽(calcitonin gene-related peptide,CGRP)对人牙髓细胞促矿化功能的影响,探讨CGRP在牙髓炎症状态下表达量增多的生物学意义。方法:人牙髓细胞分实验组和对照组培养,实验组加入适量的CGRP。分别测定细胞的碱性磷酸酶活性、骨钙素含量、I型胶原mRNA表达量变化。结果:培养3、6、9、12、15d,5个时间点实验组比对照组细胞碱性磷酸酶活性增强、骨钙素含量增加,且有显著性差异(P<0.01)。培养6d的实验组的细胞I型胶原mRNA表达比对照组明显高。结论:CGRP刺激牙髓细胞分化,促进矿化形成,CGRP表达增高将有助于修复性牙本质形成。  相似文献   
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Background

Endothelial glycocalyx regulates the endothelial function and plays an active role in maintaining vascular homeostasis. During ischema and reperfusion, the glycocalyx is rapidly shed into the blood stream. A Corline heparin conjugate (CHC; Corline systems AB, Uppsala, Sweden) consists of 70 heparin molecules that have the capacity to adhere strongly to biological tissues expressing heparin affinity. We hypothesized that CHC could be used to restore disrupted glycocalyx in vivo in kidneys from brain-dead pigs.

Materials and methods

Brain death was induced in male landrace pigs (n = 6) by inflating a balloon catheter in the epidural space until obtaining negative cerebral perfusion. The recovered kidneys (n = 5 + 5) were perfused by hypothermic machine perfusion using two Lifeport kidney transporters (Organ Recovery Systems, Chicago, IL). CHC (50 mg) (including 25 mg biotinylated CHC) or 50 mg unfractionated heparin (control) was added to the perfusion fluid in the respective machines. In one case, the kidneys were used only for dose escalation of CHC with the same procedure.

Results

CHC was detected by immunofluorescence and confocal microscopy in the inner surface of the vessel walls. The binding of CHC in the kidney was confirmed indirectly by consumption of CHC from the perfusion fluid.

Conclusions

In this first attempt, we show that CHC maybe used to coat the vessel walls of perfused kidneys during hypothermic machine perfusion, an approach that could become useful in restoring endothelial glycocalyx of kidneys recovered from deceased donors to protect vascular endothelium and possibly ameliorate ischemia and reperfusion injuries.  相似文献   
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目的探讨缺氧条件下人脐静脉内皮细胞(human umbilical vein endothelial cell,HUVEC)中长链非编码RNA(long non-coding RNA,lnc RNA)LINC01116的表达及其在炎症分子表达调控中的作用。方法采用三气培养箱模拟缺氧环境(1%O_2),常氧对照组细胞于普通培养箱(21%O_2)中常规培养。采用实时荧光定量PCR检测LINC01116及各炎症分子的m RNA水平。Western blot检测缺氧诱导因子-1α(hypoxia-inducible factor 1 alpha,HIF-1α)蛋白水平,并用葡萄糖转运体-1(glucose transporter 1,GLUT-1)的转录表达水平反映HIF-1的转录活性。免疫荧光法检测核转录因子NF-κB(nuclear factor of kappa B,NF-κB)活性亚基p65在细胞中的分布,并计算p65入核的细胞比例。结果 q RT-PCR的结果显示,缺氧条件下,LINC01116在HUVEC中持续高表达,与常氧对照组相比,差异均具有统计学意义(P<0.01)。经脯氨酸羟化酶抑制剂(DMOG)和去铁酰胺(DFX)处理后,常氧培养HUVEC中HIF-1α蛋白表达和GLUT-1的转录表达增加,LINC01116表达增高,与溶剂对照组相比,差异均具有统计学意义(P<0.01)。经YC-1和小干扰RNA处理后,缺氧培养HUVEC中HIF-1α蛋白表达和GLUT-1的转录表达下降,LINC01116的表达显著下降,与各对照组相比,差异均具有统计学意义(P<0.01)。缺氧24 h时,HUVEC中炎症分子TNF-α、IL-1β、ICAM、E-SELECTIN的m RNA水平增加,干扰LINC01116表达后,上述炎症分子的m RNA水平显著降低(P<0.01)。免疫荧光的实验显示,缺氧24 h后,细胞核内p65的分布增加,而干扰LINC01116表达后,p65入核的细胞比例下降,与对照组相比,差异均具有统计学意义(P<0.05)。结论缺氧通过HIF-1途径诱导血管内皮细胞LINC01116的表达增加;LINC01116可以通过调控p65入核,调节内皮细胞炎症分子的表达,参与介导缺氧血管内皮细胞炎症反应。  相似文献   
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