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1.
Cathryn M. Kolka 《Clinical and experimental pharmacology & physiology》2020,47(1):168-175
The endocrine system relies on the vasculature for delivery of hormones throughout the body, and the capillary microvasculature is the site where the hormones cross from the blood into the target tissue. Once considered an inert wall, various studies have now highlighted the functions of the capillary endothelium to regulate transport and therefore affect or maintain the interstitial environment. The role of the capillary may be clear in areas where there is a continuous endothelium, yet there also appears to be a role of endothelial cells in tissues with a sinusoidal structure. Here we focused on the most common endocrine disorder, diabetes, and several of the target organs associated with the disease, including skeletal muscle, liver and pancreas. However, it is important to note that the ability of hormones to cross the endothelium to reach their target tissue is a component of all endocrine functions. It is also a consideration in organs throughout the body and may have greater impact for larger hormones with target tissues containing a continuous endothelium. We noted that the blood levels do not always equal interstitial levels, which is what the cells are exposed to, and discussed how this may change in diseases such as obesity and insulin resistance. The capillary endothelium is, therefore, an essential and understudied aspect of endocrinology and metabolism that can be altered in disease, which may be an appropriate target for treatment. 相似文献
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为了探明血管内皮细胞在急性低无性肺动脉高压中的作用进行了本研究。雄性SD大鼠经20%乌拉坦麻醉,气管插管,呼吸机通气。动物分为两组:单纯低氧组(n=10只)吸10.5%低氧混合气体5分钟;另一组为肺损伤低无组(n=7只),ANTUlmg/kg缓慢注入肺动脉内,再吸入10.5%低氧混合气体。实验结果表明:大鼠吸入低氧混合气体后肺动脉平均压PPa)增加20.4±6.5%,而肺损伤后再吸入低氧气体,PPa仅增加8.7±3.8%,显著低于单纯低氧组(P<0.01).结果提示:血管内皮细胞受损后急性低氧性肺血管收缩反应明显减弱。 相似文献
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本文报道了一种显露内皮下层纤维连接素的理想方法。大白鼠主动脉壁分别用1.0%NP-40作用5min,30.0mmol/L KCl作用10min后,内皮细胞全部脱离,内皮下层大部分纤维连接素被保留。本法适用于建立细胞与血管壁相互作用的体外实验模型。 相似文献
7.
目的:探讨外周血循环内皮细胞(CEC)和糖尿病肾病(DN)的相关性,以及银杏达莫注射液在DN防治中的可能作用。方法:检测65例2型糖尿病患者24h尿白蛋白排泄率(UAER)及CEC数,分析两者的相关性。将UAER为30~300mg·d-1的45例患者随机分为两组,常规治疗组22例,进行常规降血糖、控制血压等治疗;银杏达莫治疗组23例,在常规治疗基础上静脉滴注银杏达莫注射液2周。比较两组治疗前后血糖、血压、UAER及CEC水平的变化。结果:单纯糖尿病(SDM)组和早期糖尿病肾病(EDN)组的外周血CEC水平比对照组(NC)显著性升高,并呈逐渐增高的趋势(P<0.01)。UAER与收缩压(SBP)、外周血CEC水平呈正相关(P<0.01)。EDN组中,银杏达莫治疗后UAER及CEC明显降低(P<0.01);而常规治疗组无明显变化。线性多元逐步回归分析表明,银杏达莫治疗后UAER的改变与CEC数的变化成正相关(P<0.01)。结论:血管内皮细胞(VEC)损伤在DN发生发展中起重要作用,银杏达莫对VEC的保护作用可能是其延缓DN发展的重要机制。 相似文献
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本实验采用血管内皮细胞培养模型,动态观察了家兔烧伤(30%Ⅲ度)早期烧伤表对内皮细胞结构和功能的影响,通过相差显微动态观察、台盘菜染色、HE染色光镜检查及扫描电镜观察。同时检测孵育不同时相点增减液中LDH、6-keto-PGE1α、tPA及内皮细胞抗上板粘附能力变化。结果显示:(1)烧伤血清对内皮细胞有明显的损伤作用功能改变早于结构损害,而结构损害又以细胞间连接及其表达结构改变为早;(2)烧伤血 相似文献
9.
Chronic vitamin E treatment prevents defective endothelium-dependent relaxation in diabetic rat aorta 总被引:2,自引:2,他引:0
Summary We examined the effect in rats of 2 months of streptozotocin-induced diabetes mellitus on relaxation and contraction of aortas in vitro. A further diabetic group was treated from time of diabetes induction with a 1% dietary supplement of vitamin E. Diabetes caused a 26.5% deficit (p<0.001) in maximum endothelium-dependent relaxation to acetylcholine in phenylephrine-precontracted aortas. This was 64.3% attenuated (p<0.01) by vitamin E treatment; maximum relaxation was not significantly altered compared to non-diabetic rats. Vitamin E treatment of non-diabetic rats did not significantly affect acetylcholine-induced relaxation. Diabetes or treatment did not significantly alter acetylcholine sensitivity. Endothelium-independent relaxation response to glyceryl trinitrate was not affected by diabetes or vitamin E treatment, indicating that vascular smooth muscle responses to nitric oxide remained unaltered. There was a 35.4% reduction in the maximum contractile response to phenylephrine with diabetes (p<0.05) which was unaffected by vitamin E treatment. The data suggest that the chronic deficit in nitric oxide-mediated endothelium-dependent relaxation in diabetes depends largely upon excess activity of reactive oxygen species. Treatment with vitamin E to increase free radical scavenging specifically protected vascular endothelium although it had no effect on deficits in vascular smooth muscle contractile responses.Abbreviations NO
Nitric oxide
- ARI
aldose reductase inhibitor
- ACH
acetylcholine
- GTN
glyceryl trinitrate
- GSH
reduced form of glutathione
- EC50
effective concentration for 50% of the maximal response 相似文献
10.
Gary Coleman Tom A. Gardiner Ariel Boutaud Alan W. Stitt 《Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie》2007,245(4):581-587
Background A recombinant form of the α2(IV)NC1 domain of type IV collagen has been shown to have potent anti-angiogenic activity although
this peptide has not been studied in the context of proliferative retinopathies. In the current investigation we examined
the potential for α2(IV)NC1 to regulate retinal microvascular endothelial cell function using a range of in vitro and in vivo
assay systems.
Materials and methods α2(IV)NC1 at concentrations between 0.1 and 1 μg/ml was added to retinal microvascular endothelial cells (RMECs) followed
by assessment of cell attachment, proliferation and survival. This agent was also tested within a novel in vitro three-dimensional
retinal angiogenesis assay and the number of angiogenic sprouts quantified. α2(IV)NC1 was also delivered intra-vitreally to
mice with oxygen-induced proliferative retinopathy (OIR) and neovascularisation evaluated in comparison with vehicle-treated
controls.
Results RMECs treated with α2(IV)NC1 (0.1, 0.5 and 1 μg/ml) showed delayed attachment at 3 h post-seeding, although this deficit had
been restored at the 6-h time point. BrdU assay of DNA replication revealed that confluent RMECs treated with α2(IV)NC1 showed
no measurable response in comparison with vehicle-treated controls. By contrast, proliferation of sub-confluent RMECs was
significantly reduced by α2(IV)NC1 at 0.5 μg/ml (P<0.01). α2(IV)NC1 also induced apoptosis in RMECs and inhibited angiogenesis of pre-existing retinal vascular networks in
vitro (P<0.001). Intra-vitreal injection of α2(IV)NC1 in the OIR model significantly inhibited pre-retinal neovascularisation compared
with vehicle-treated controls (P<0.001).
Conclusion α2(IV)NC1 inhibits angiogenesis in the retinal microvasculature. This recombinant protein has potential for the treatment
of neovascularisation in proliferative retinopathies.
BioStratum Inc. did not sponsor this research in any way. None of the authors are paid consultants with this company. 相似文献