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排序方式: 共有985条查询结果,搜索用时 15 毫秒
61.
62.
Restenosis rates following bifurcation stenting with sirolimus-eluting stents for de novo narrowings 总被引:7,自引:0,他引:7
Tanabe K Hoye A Lemos PA Aoki J Arampatzis CA Saia F Lee CH Degertekin M Hofma SH Sianos G McFadden E Smits PC van der Giessen WJ de Feyter P van Domburg RT Serruys PW 《The American journal of cardiology》2004,94(1):115-118
The percutaneous treatment of coronary bifurcation stenoses is hampered by an increased rate of subsequent restenosis. The present study reports on the outcomes of a consecutive series of 58 patients with 65 de novo bifurcation stenoses treated with sirolimus-eluting stent implantation in both the main vessel and side branch. At 6 months, the incidence of major adverse cardiac events was 10.3% (1 death and 5 target lesion revascularizations) with no episodes of acute myocardial infarction or stent thrombosis. 相似文献
63.
64.
Pneumocystis carinii pneumonia studied by gallium-67 scanning 总被引:1,自引:0,他引:1
The validity and reliability of gallium-67 (Ga-67) scanning for diagnosis and follow-up of Pneumocystis carinii pneumonia (PCP) were assessed in 34 patients thought to have pulmonary complications of acquired immunodeficiency syndrome (AIDS). Overall sensitivity was 94% and specificity 74%. Among patients with normal or equivocal chest radiographs at the time of admission, sensitivity was 86% and specificity 85%. The authors consider Ga-67 scanning a valid and reliable adjunct in the diagnosis of PCP in AIDS patients with respiratory symptoms when the chest radiograph is normal or equivocal. 相似文献
65.
葛根素对高血压患者血浆内皮素和一氧化氮的影响 总被引:29,自引:0,他引:29
目的:检测正常人与高血压病(EH)患者血浆内皮素、一气体氮的变化及葛根素对其的干预效应。方法:EH对照组口服苯磺酸氨氯地平5mg/d,或合和盐酸苯那普利10mg/d,每日一次,15d为一疗程。EH伍用治疗组同时合用5%GNS250ml+葛根素注射液400mg静滴,两组治疗前后检测血浆ET、NO水平变化。结果:EH各组血浆ET较正常人组均显著增高(P〈0.01),血浆NO水平及NO/ET比值除轻度E 相似文献
66.
67.
68.
Liu SC; Palek J; Yi SJ; Nichols PE; Derick LH; Chiou SS; Amato D; Corbett JD; Cho MR; Golan DE 《Blood》1995,86(1):349-358
Southeast Asian ovalocytosis (SAO) is an asymptomatic trait characterized by rigid, poorly deformable red cells that resist invasion by several strains of malaria parasites. The underlying molecular genetic defect involves simple heterozygous state for a mutant band 3 protein, which contains a deletion of amino acids 400 through 408, linked with a Lys 56-to-Glu substitution (band 3-Memphis polymorphism). To elucidate the contribution of the mutant SAO band 3 protein to increased SAO red blood cell (RBC) rigidity, we examined the participation of the mutant SAO band 3 protein in increased band 3 attachment to the skeleton and band 3 oligomerization. We found first that SAO RBC skeletons retained more band 3 than normal cells and that this increased retention preferentially involved the mutant SAO band 3 protein. Second, SAO RBCs contained a higher percentage of band 3 oligomer-ankyrin complexes than normal cells, and these oligomers were preferentially enriched by the mutant SAO protein. At the ultrastructural level, the increased oligomer formation of SAO RBCs was reflected by stacking of band 3-containing intramembrane particles (IMP) into longitudinal strands. The IMP stacking was not reversed by treating SAO RBCs in alkaline pH (pH 11), which is known to weaken ankyrin-band 3 interactions, or by removing the cytoplasmic domain of band 3 from SAO membranes with trypsin. Finally, we found that band 3 protein in intact SAO RBCs exhibited a markedly decreased rotational mobility, presumably reflecting the increased oligomerization and the membrane skeletal association of the SAO band 3 protein. We propose that the mutant SAO band 3 has an increased propensity to form oligomers, which appear as longitudinal strands of IMP and exhibit increased association with membrane skeleton. This band 3 oligomerization underlies the increase in membrane rigidity by precluding membrane skeletal extension, which is necessary for membrane deformation. 相似文献
69.
Arlin ZA; Fanucchi MP; Gee TS; Kempin SJ; Mertelsmann R; Young CW; Clarkson BD 《Blood》1982,60(5):1224-1226
Twenty-four adults with ALL were treated with AMSA alone or in combination. Twenty-two were treated at time of relapse and two patients after failing primary induction therapy. All had been treated with anthracyclines prior to receiving AMSA. Of the 22 patients with ALL in relapse, 4 achieved a complete remission. Two of these patients have relapsed while receiving maintenance chemotherapy; one died 1 mo after achieving remission due to the occurrence of cholycystitis in the setting of pancytopenia and one patient underwent bone marrow transplantation and is in remission at 8 mo after the second remission. Both patients who failed primary induction therapy remain in remission at 11 and 36 mo, respectively. The use of AMSA should be considered for patients with ALL who fail primary induction as well as those whose leukemia becomes resistant to conventional agents. 相似文献
70.
CTLA-4 is required for the induction of high dose oral tolerance 总被引:5,自引:3,他引:5
Samoilova EB; Horton JL; Zhang H; Khoury SJ; Weiner HL; Chen Y 《International immunology》1998,10(4):491-498
Mucosal and systemic administrations of high dose antigens induce long-
lasting peripheral T cell tolerance. We and others have shown that high
dose peripheral T cell tolerance is mediated by anergy or deletion and is
preceded by T cell activation. Co-stimulatory molecules B7-1 (CD80)/B7-2
(CD86) and their counter-receptors CD28/CTLA-4 play pivotal roles in T cell
activation and immune regulation. In the present study, we examined the
roles of the B7 co-stimulation pathway in the generation of high dose
peripheral T cell tolerance. We found that blocking B7:CD28/CTLA-4
interaction at the time of tolerance induction partially prevented T cell
tolerance, whereas selective blockade of B7:CTLA-4 interaction completely
abrogated peripheral T cell tolerance induced by either oral or i.p.
antigens. These results suggest that CTLA-4-mediated feedback regulation
plays a crucial role in the induction of high dose peripheral T cell
tolerance.
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