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排序方式: 共有782条查询结果,搜索用时 15 毫秒
1.
Alexander Stoff MD ; Angel A. Rivera PhD ; N. S. Banerjee PhD ; J. Michael Mathis PhD ; Antonio Espinosa-de-los-Monteros MD ; Long P. Le PhD ; Jorge I. De la Torre MD ; Luis O. Vasconez MD ; Thomas R. Broker PhD ; Dirk F. Richter MD ; Mariam A. Stoff-Khalili MD ; David T. Curiel MD PhD 《Wound repair and regeneration》2006,14(5):608-617
Genetically modified keratinocytes and fibroblasts are suitable for delivery of therapeutic genes capable of modifying the wound healing process. However, efficient gene delivery is a prerequisite for successful gene therapy of wounds. Whereas adenoviral vectors (Ads) exhibit superior levels of in vivo gene transfer, their transductional efficiency to cells resident within wounds may nonetheless be suboptimal, due to deficiency of the primary adenovirus receptor, coxsackie-adenovirus receptor (CAR). We explored CAR-independent transduction to fibroblasts and keratinocytes using a panel of CAR-independent fiber-modified Ads to determine enhancement of infectivity. These fiber-modified adenoviral vectors included Ad 3 knob (Ad5/3), canine Ad serotype 2 knob (Ad5CAV-2), RGD (Ad5.RGD), polylysine (Ad5.pK7), or both RGD and polylysine (Ad5.RGD.pK7). To evaluate whether transduction efficiencies of the fiber-modified adenoviral vectors correlated with the expression of their putative receptors on keratinocytes and fibroblasts, we analyzed the mRNA levels of CAR, alpha upsilon integrin, syndecan-1, and glypican-1 using quantitative polymerase chain reaction. Analysis of luciferase and green fluorescent protein transgene expression showed superior transduction efficiency of Ad5.pK7 in keratinocytes and Ad5.RGD.pK7 in fibroblasts. mRNA expression of alpha upsilon integrin, syndecan-1 and glypican-1 was significantly higher in primary fibroblasts than CAR. In keratinocytes, syndecan-1 expression was significantly higher than all the other receptors tested. Significant infectivity enhancement was achieved in keratinocytes and fibroblasts using fiber-modified adenoviral vectors. These strategies to enhance infectivity may help to achieve higher clinical efficacy of wound gene therapy. 相似文献
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一些保肝药物对原代培养大鼠肝细胞糖原合成功能的影响 总被引:1,自引:0,他引:1
本文参照PO Seglen的方法并加以修改,建立了原代培养大鼠肝细胞糖原合成功能的测定体系。观察到联苯双酯既能使正常肝细胞合成糖原增加88%,又能保护肝细胞完全拮抗四氯化碳对其功能的损伤;银耳多糖能使四氯化碳对肝细胞糖原合成功能的损伤减轻57%;去甲斑蝥素10μg/ml能增加肝细胞糖原合成,浓度增加到100μg/ml时,此作用减弱,1000μg/ml则明显抑制糖原的合成,而且在10~100μg/ml浓度时,即能加强四氯化碳的损伤作用;100μg/ml CL1500和熊果酸二钠单独应用可增加肝细胞糖原合成,但与四氯化碳同时应用,反而加重对糖原合成的抑制作用。 相似文献
5.
Neulen J; Raczek S; Pogorzelski M; Grunwald K; Yeo TK; Dvorak HF; Weich HA; Breckwoldt M 《Molecular human reproduction》1998,4(3):203-206
Vascularization is a prominent event during corpus luteum formation,
providing low density lipoproteins for steroid biosynthesis and enabling
transport of secreted steroids. The process of vascularization is
controlled by specific regulators. Vascular endothelial growth factor
(VEGF), otherwise named vascular permeability factor (VPF), induces
endothelial cell proliferation as well as angiogenesis in vivo and
increases capillary permeability. Here we report the expression of VEGF/VPF
mRNA by cultured human luteinized granulosa cells (GC) for at least 10
days. Without HCG VEGF/VPF expression declined after day 4 and by day 10
was reduced to approximately 30% of the value at day 4. However, after
culture in the presence of 1 U/ml human chorionic gonadotrophin (HCG),
expression of VEGF/VPF mRNA by GC was four times greater than control
experiments by day 10, and increased 100% from day 4 to day 10.
Simultaneously, HCG supplementation increased VEGF/VPF secretion by GC.
Medium VEGF/VPF on day 3 was 13 pM without and 11 pM with HCG. Medium
VEGF/VPF on day 10 was 6 pM without HCG and 29 pM with HCG. These results
suggest that vascularization of the corpus luteum is induced by
HCG-mediated effects of VEGF/VPF.
相似文献
6.
The UTX gene escapes X inactivation in mice and humans 总被引:7,自引:3,他引:7
Greenfield A; Carrel L; Pennisi D; Philippe C; Quaderi N; Siggers P; Steiner K; Tam PP; Monaco AP; Willard HF; Koopman P 《Human molecular genetics》1998,7(4):737-742
We recently have identified a ubiquitously transcribed mouse Y chromosome
gene, Uty , which encodes a tetratricopeptide repeat (TPR) protein. A
peptide derived from the UTY protein confers H-Y antigenicity on male
cells. Here we report the characterization of a widely transcribed X-linked
homologue of Uty , called Utx , which maps to the proximal region of the
mouse X chromosome and which detects a human X-linked homologue at Xp11.2.
Given that Uty is ubiquitously transcribed, we assayed for Utx expression
from the inactive X chromosome (Xi) in mice and found that Utx escapes X
chromosome inactivation. Only Smcx and the pseudoautosomal Sts gene on the
mouse X chromosome have been reported previously to escape inactivation.
The human UTX gene was also found to be expressed from Xi. We discuss the
significance of these data for our understanding of dosage compensation of
X-Y homologous genes in humans and mice.
相似文献
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Tissue and lineage-specific variation in inactive X chromosome expression of the murine Smcx gene 总被引:2,自引:0,他引:2
To understand how gene expression patterns are established on the inactive
X chromosome during development, we have studied the murine gene Smcx,
which is expressed from both the active and inactive mouse X chromosomes.
In all tissues assayed, Smcx only partially escapes X inactivation, with
expression levels from the inactive X allele approximately 30-65% that of
the active X allele. Additionally, inactive X expression levels differed
between extraembryonic and embryonic tissues and among different tissues
from newborn and adult mice. Imprinted extraembryonic tissue had the lowest
levels of inactive X Smcx expression, whereas the highest levels were in
heart. These data suggest that the chromosomal basis of X inactivation
differs among tissues, perhaps reflecting differences in the timing or
regulation of inactivation in these cell lineages.
相似文献
9.
Dendritic cells generated in the presence of GM-CSF plus IL-15 prime potent CD8+ Tc1 responses in vivo 总被引:7,自引:0,他引:7
Pulendran B Dillon S Joseph C Curiel T Banchereau J Mohamadzadeh M 《European journal of immunology》2004,34(1):66-73
Dendritic cells (DC) comprise a system of professional antigen-presenting cells, which induce the stimulation of very rare antigen-specific naive T cells. DC progenitors can be stimulated to differentiate into immature DC by various growth factors, including GM-CSF and IL-4. Here we show that IL-15, in combination with GM-CSF, is a growth factor for murine DC. Murine bone marrow cells, depleted of T cells, B cells, I-A+ cells and Gr-1+ granulocytes, and cultured in the presence of GM-CSF plus IL-15 (IL-15 DC), yielded DC expressing high levels of CD11c and MHC class II molecules, as well as CD11b. These cells expressed significant levels of CD40, CD80 and CD86, and could stimulate allogeneic CD4+ T cells efficiently. Interestingly, IL-15 DC were far superior to DC generated with GM-CSF plus IL-4 in stimulating allogeneic CD8+ T cells in vitro. Consistent with this, IL-15 DC induced much more potent antigen-specific CD8+ T cell responses with high levels of Th1 cytokines in vivo, compared to DC generated with GM-CSF plus IL-4, or with GM-CSF plus TGF-beta, or with GM-CSF alone. Together, these data suggest that IL-15 promotes the development of DC, which induce potent Th1 and Tc1 responses in vivo. This suggests potential roles for these IL-15 DC cells in the immunotherapy of tumors and infectious diseases. 相似文献
10.
Dal Zotto L; Quaderi NA; Elliott R; Lingerfelter PA; Carrel L; Valsecchi V; Montini E; Yen CH; Chapman V; Kalcheva I; Arrigo G; Zuffardi O; Thomas S; Willard HF; Ballabio A; Disteche CM; Rugarli EI 《Human molecular genetics》1998,7(3):489-499
We have recently reported isolation of the gene responsible for X- linked
Opitz G/BBB syndrome, a defect of midline development. MID1 is located on
the distal short arm of the human X chromosome (Xp22. 3) and encodes a
novel member of the B box family of zinc finger proteins. We have now
cloned the murine homolog of MID1 and performed preliminary expression
studies during development. Mid1 expression in undifferentiated cells in
the central nervous, gastrointestinal and urogenital systems suggests that
abnormal cell proliferation may underlie the defect in midline development
characteristic of Opitz syndrome. We have also found that Mid1 is located
within the mouse pseudoautosomal region (PAR) in Mus musculus , while it
seems to be X- specific in Mus spretus. Therefore, Mid1 is likely to be a
recent acquisition of the M. musculus PAR. Genetic and FISH analyses also
demonstrated a high frequency of unequal crossovers in the murine PAR,
creating spontaneous deletion/duplication events involving Mid1. These data
provide evidence for the first time that genetic instability of the PAR may
affect functionally important genes. In addition, we show that MID1 is the
first example of a gene subject to X-inactivation in man while escaping it
in mouse. These data contribute to a better understanding of the molecular
content and evolution of the rodent PAR.
相似文献