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A study was carried out which compared how two groups of people, one with clinical dental experience and one without, assessed restorative dental treatment need. Using a visual analogue scale, a group of final year dental students ( n = 50) and nonclinical university students ( n = 50) assessed the extent to which they considered common dental imperfections, viz. spacing of the upper anterior teeth and discolouration of upper anterior teeth, warranted restorative correction. The group of dental students judged the necessity for treatment of discolouration to be more urgent than correction of spacing. The nondental group did not differentiate between the degrees of need. Data were non‐normal in distribution but the use of appropriate statistical tests showed the differences in mean assessments to be significant. 相似文献
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Mutations in the retinal guanylate cyclase (RETGC-1) gene in dominant cone-rod dystrophy 总被引:3,自引:0,他引:3
Kelsell RE; Gregory-Evans K; Payne AM; Perrault I; Kaplan J; Yang RB; Garbers DL; Bird AC; Moore AT; Hunt DM 《Human molecular genetics》1998,7(7):1179-1184
The dominant cone-rod dystrophy gene CORD6 has previously been mapped to
within an 8 cM interval on chromosome 17p12-p13. The retinal- specific
guanylate cyclase gene (RETGC-1), which maps to within this genetic
interval and previously was implicated in Leber's congenital amaurosis, was
screened for mutations within this family and in a panel of small families
and individuals with various cone and cone- rod dystrophy phenotypes. A
missense mutation (E837D) was identified in affected members of the CORD6
family, as well as a second missense mutation (R838C) in three other
families with dominant cone-rod dystrophy. RETGC-1 is only the fourth gene
to be implicated in cone-rod dystrophy and this is the first report of
dominant mutations in this gene.
相似文献
15.
Injection of soluble protein antigen into the anterior chamber of the eye
of primed mice induces anterior chamber-associated immune deviation (ACAID)
which is manifested by suppression of delayed-type hypersensitivity (DTH)
to the antigen. Recently, we found that ACAID induced in primed mice also
results in a rapid rise in serum of soluble T lymphocyte-derived proteins
specific for nominal antigen (TABM). Here, we demonstrate that serum TABM
induced in primed mice during ACAID will transfer the suppression of DTH to
mice primed to the same antigen. Sera from TNP-BSA-primed mice that
received an anterior chamber injection of TNP-BSA, but not BSA alone,
suppressed the DTH response to TNP when injected into other TNP-BSA-primed
mice. Sera absorbed with Sepharose beads conjugated with either anti-TCR
C(alpha), anti-TCR C(beta), anti-TABM or TNP-BSA did not contain
TNP-specific TABM and did not transfer suppression of DTH. These results
suggest that the antigen-specific, TCR C(alphabeta)+ TABM that appear in
serum during ACAID are able to confer on or amplify the capacity of
sensitized T cells to suppress DTH. We believe this to be the first
demonstration of an in vivo immunologic function that is specifically
associated with TABM produced in vivo.
相似文献
16.
IL-10-driven immunoglobulin production by B lymphocytes from IgA-deficient individuals correlates to infection proneness 下载免费PDF全文
V FRIMAN L HANSON J-M BRIDON A TARKOWSKI J BANCHEREAU F BRIRE 《Clinical and experimental immunology》1996,104(3):432-438
In search for a possible explanation of the phenotypic heterogeneity in IgA deficiency, we studied the function of B cells from IgA-deficient (IgAd) individuals. Two groups of IgAd individuals, one frequently infected and one clinically apparently healthy, as well as normal controls, were studied. Peripheral blood mononuclear cells (PBMC) and B cells from IgAd individuals and controls were cultured with Staphylococcus aureus Cowan I strain and with anti-CD40 MoAb presented on the CD32-transfected fibroblast cell line in the presence of IL-10. In this experimental system PBMC and B cells from the infection-prone IgAd individuals produced only minute amounts of IgA. In contrast, PBMC and B cells from healthy IgAd subjects secreted significantly more IgA1 and IgA2 in comparison with infection-prone IgAd patients (P < 0.05). These data suggest that the abnormalities of B cell differentiation in IgAd could be of heterogeneous origin. Thus, whereas in healthy IgAd subjects IgA production may be efficiently up-regulated in vitro by addition of IL-10 to CD40-activated B cell culture, the corresponding B cell differentiation does not occur in infection-prone IgAd patients. These observations provide a conceptual framework for phenotypic heterogeneity in IgAd subjects. 相似文献
17.
R. Blazev M. Hussain A.J. Bakker S.I. Head G.D. Lamb 《Journal of muscle research and cell motility》2001,22(3):277-286
This study investigated the effects of the protein kinase A (PKA) inhibitor, H-89, in mechanically-skinned muscle fibres and intact muscle fibres, in order to determine whether PKA phosphorylation is essential for normal excitation–contraction (E–C) coupling. In skinned EDL fibres of the rat, force responses to depolarization (by ion substitution) were inhibited only slightly by 10M H-89, a concentration more than sufficient to fully inhibit PKA. Staurosporine (1 M), a potent non-specific kinase inhibitor, also had little if any effect on depolarization-induced responses. At 1–2 M, H-89 significantly slowed the repriming rate in rat skinned fibres, most likely due to it deleteriously affecting the T-system potential. With 100 M H-89, the force response to depolarization by ion substitution was completely abolished. This inhibitory effect was reversed by washout of H-89 and was not due to block of the Ca2+ release channel in the sarcoplasmic reticulum (SR). In intact single fibres of the flexor digitorum longus (FDB) muscle of the mouse, 1–3 M H-89 had no noticeable effect on action-potential-mediated Ca2+ transients. Higher concentrations (4–10 M) caused Ca2+ transient failure in fibres stimulated at 20 Hz in a manner indicative of action-potential failure. At 10–100 M, H-89 also inhibited net Ca2+ uptake by the SR and affected the Ca2+-sensitivity of the contractile apparatus in rat skinned fibres. All such effects were proportionately greater in toad muscle fibres. These results do not support the hypothesis that phosphorylation is essential for the Ca2+ release channel to open in response to voltage-sensor activation in skeletal muscle fibres. 相似文献
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Requirements for the development of IL-4-producing T cells during intestinal nematode infections: what it takes to make a Th2 cell in vivo 总被引:1,自引:0,他引:1
Zhugong Liu Qian Liu John Pesce Robert M. Anthony Erika Lamb Jeannette Whitmire Hossein Hamed Motoko Morimoto Joseph F. Urban Jr William C. Gause 《Immunological reviews》2004,201(1):57-74
Summary: Components of the type 2 immune response may mediate host protection against both helminthic parasites and harmful allergic responses. A central player in this response is the T‐helper 2 (Th2) effector cell, which produces interleukin (IL)‐4, IL‐5, IL‐13, and other Th2 cytokines during the primary and memory response. Specific aspects of the parasite that trigger Th2‐cell differentiation are not yet defined. Furthermore, the cell types and cell surface and secreted molecules that provide the immune milieu required for the development of Th2 effector cells and also Th2 memory cells are not well understood. They will probably vary with the particular helminth or other antigen inducing the Th2 response. We have used third stage larvae of intestinal nematode parasites as adjuvants to promote naïve nonparasite antigen‐specific T cells to differentiate into Th2 cells. This model system avoids possible parasite antigen‐specific T‐cell clones or cross‐reactive memory T cells that may preferentially differentiate into Th2 effector cells during the course of infection and confound the stereotypical components of parasite‐induced Th2 cell differentiation. We have found that these parasites have a potent adjuvant effect and have used our model system to begin to investigate the events that lead to the development of polarized Th2 cells in vivo. 相似文献
20.