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排序方式: 共有326条查询结果,搜索用时 15 毫秒
91.
Human platelet surface binding of endogenous secreted factor VIII-von Willebrand factor and platelet factor 4 总被引:6,自引:0,他引:6
Washed human platelets in buffers containing either 2 mM Ca++ or 4 mM EDTA were stimulated by human alpha-thrombin to induce secretion. The binding of two endogenous secreted proteins, factor-VIII-related protein (VIII-R) (von Willebrand factor) and platelet factor 4, was measured by reacting thrombin-treated and control platelets with specific antibodies to these proteins, then quantifying antibody binding with 125I-staphylococcal protein A. Both of these granule proteins were associated with the platelet membrane surface by a calcium-dependent mechanism after thrombin-induced secretion. This ability to bind endogenous secreted proteins to the plasma membrane surface may provide a mechanism by which the platelet can concentrate and organize its secreted proteins for subsequent physiologic reactions. 相似文献
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Lehnart SE Ackerman MJ Benson DW Brugada R Clancy CE Donahue JK George AL Grant AO Groft SC January CT Lathrop DA Lederer WJ Makielski JC Mohler PJ Moss A Nerbonne JM Olson TM Przywara DA Towbin JA Wang LH Marks AR 《Circulation》2007,116(20):2325-2345
The National Heart, Lung, and Blood Institute and Office of Rare Diseases at the National Institutes of Health organized a workshop (September 14 to 15, 2006, in Bethesda, Md) to advise on new research directions needed for improved identification and treatment of rare inherited arrhythmias. These included the following: (1) Na+ channelopathies; (2) arrhythmias due to K+ channel mutations; and (3) arrhythmias due to other inherited arrhythmogenic mechanisms. Another major goal was to provide recommendations to support, enable, or facilitate research to improve future diagnosis and management of inherited arrhythmias. Classifications of electric heart diseases have proved to be exceedingly complex and in many respects contradictory. A new contemporary and rigorous classification of arrhythmogenic cardiomyopathies is proposed. This consensus report provides an important framework and overview to this increasingly heterogeneous group of primary cardiac membrane channel diseases. Of particular note, the present classification scheme recognizes the rapid evolution of molecular biology and novel therapeutic approaches in cardiology, as well as the introduction of many recently described diseases, and is unique in that it incorporates ion channelopathies as a primary cardiomyopathy in consensus with a recent American Heart Association Scientific Statement. 相似文献
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Drew C Deniger Kirsten Switzer Tiejuan Mi Sourindra Maiti Lenka Hurton Harjeet Singh Helen Huls Simon Olivares Dean A Lee Richard E Champlin Laurence JN Cooper 《Molecular therapy》2013,21(3):638-647
Even though other γδ T-cell subsets exhibit antitumor activity, adoptive transfer of γδ Tcells is currently limited to one subset (expressing Vγ9Vδ2 T-cell receptor (TCR)) due to dependence on aminobisphosphonates as the only clinically appealing reagent for propagating γδ T cells. Therefore, we developed an approach to propagate polyclonal γδ T cells and rendered them bispecific through expression of a CD19-specific chimeric antigen receptor (CAR). Peripheral blood mononuclear cells (PBMC) were electroporated with Sleeping Beauty (SB) transposon and transposase to enforce expression of CAR in multiple γδ T-cell subsets. CAR+γδ T cells were expanded on CD19+ artificial antigen-presenting cells (aAPC), which resulted in >109 CAR+γδ T cells from <106 total cells. Digital multiplex assay detected TCR mRNA coding for Vδ1, Vδ2, and Vδ3 with Vγ2, Vγ7, Vγ8, Vγ9, and Vγ10 alleles. Polyclonal CAR+γδ T cells were functional when TCRγδ and CAR were stimulated and displayed enhanced killing of CD19+ tumor cell lines compared with CARnegγδ T cells. CD19+ leukemia xenografts in mice were reduced with CAR+γδ T cells compared with control mice. Since CAR, SB, and aAPC have been adapted for human application, clinical trials can now focus on the therapeutic potential of polyclonal γδ T cells. 相似文献
96.
The excellent results obtained in this trial indicate that tinidazole is a drug worthy of extensive evaluation in the treatment of amoebiasis, as three single daily doses is a simple form of treatment. The drug was well tolerated and free from any toxic effects. 相似文献
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A 2-month-old, former 28-week premature infant with brochopulmonary dysplasia infected with respiratory syncytial virus was treated with nitric oxide and high frequency oscillatory ventilation after conventional therapy failed. Nitric oxide and high frequency oscillatory ventilation rapidly improved oxygenation allowing recovery without the need for extracorporeal membrane oxygenation. This treatment regimen should be considered as an option in high-risk infants with respiratory syncytial virus infection who meet extracorporeal membrane oxygenation criteria. 相似文献
100.
Eichler EE; Macpherson JN; Murray A; Jacobs PA; Chakravarti A; Nelson DL 《Human molecular genetics》1996,5(3):319-330
To understand the origins of the fragile X syndrome and factors
predisposing alleles to instability and hyperexpansion, we have compared
the haplotype (using markers FRAXAC1, FRAXAC2, and DXS548) and AGG
interspersion patterns of the FMR1 CGG repeat for 214 normal and 16
premutation chromosomes. Association testing between interspersion pattern
and haplotype reveals a highly significant (P < 0.002) non- random
distribution, indicating that all three markers are useful in phylogenetic
reconstruction of mutational change. Parsimony analysis of the FMR1 CGG
repeat substructure predicts that loss of AGG interruptions has occurred
independently on many haplotypes associated with the fragile X syndrome,
partially explaining the haplotype diversity of this disease. Among
haplotypes found in linkage disequilibrium with the fragile X mutation, two
different modes of mutation and predisposition to instability have been
identified. One pathway has involved the frequent and recurrent loss of AGG
interruptions from rare asymmetrical ancestral array structures.
Intergenerational transmission studies suggest that these predisposed
chromosomes progress relatively rapidly to the disease state. In contrast,
the second mutational pathway involves a single haplotype which has
maintained two AGG interruptions. Parsimony analysis of CGG repeat
substructure within this haplotype suggests that larger alleles have been
generated by gradual increments of CGG repeats distal to the most 3'
interruption. Pedigree analysis of the intergenerational stability of
alleles of this haplotype confirms a gradual progression toward instability
thresholds. As a result, a large reservoir of chromosomes carrying large
repeats on this haplotype exists. These chromosomes are predisposed to
disease. The present data support a model in which there are at least two
different mutational pathways predisposing alleles to instability and
hyperexpansion associated with the fragile X syndrome.
相似文献