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51.
Schmucker DL Owen RL Outenreath R Thoreux K 《Clinical & developmental immunology》2003,10(2-4):167-172
The elderly are characterized by mucosal immunosenescence and high rates of morbidity and mortality associated with infectious diseases of the intestinal tract. Little is known about how the differentiation of immunoglobulin A (IgA) plasma cells in Peyer's patches (PPs) and their subsequent homing to the small intestinal lamina propria (LP) is affected by aging. Quantitative immunohistochemical analyses demonstrated a 2-fold increase in the number of IgA+ cells in the PPs, coupled with significant declines in the numbers of IgA+ and antibody-positive cells in the intestinal LP of senescent rats compared to young adult animals. These data suggest that aging diminishes the emigration of IgA immunoblasts from these lymphoid aggregates, as well as their migration to the intestinal LP. Flow cytometry and lymphocyte adoptive transfer studies showed 3- to 4-fold age-related declines in the homing of antibody-containing cells and mesenteric lymph node lymphocytes to the small intestines of rhesus macaques and rats, respectively. The number of peripheral blood IgA immunoblasts expressing the homing molecule alpha4beta7 declined 30% in senescent rats. This was accompanied by a > 17% decrease in the areal density of LP blood vessels staining positive for the cell adhesion molecule MAdCAM-1. Cumulatively, declines in expression of these homing molecules constitute a substantial age-related diminution of IgA immunoblast homing potential. In vitro antibody secretion by LP plasma cells, i.e. antibody secreted per antibody-positive cell, remains unchanged as a function of donor age. Intestinal mucosal immunosenescence is a consequence of reduced homing of IgA plasma cells to the intestinal LP as a result of declines in homing molecule expression. 相似文献
52.
53.
Karine Petitprez Jean-Marie Grzych Christine Pierrot Claude Godin André Capron Jamal Khalife 《Parasitology research》1997,84(1):38-40
Genes encoding the heavy and light chains of an anti-idiotype antibody (AB2) mimicking a protective oligosaccharide of Schistosoma mansoni were cloned and expressed as a single-chain Fv fragment. The expression in a functional state was tested using the AB1. A
specific binding between sFv and AB1 was observed. Immunization with the recombinant AB2 indicates its capacity to elicit
anti-S. mansoni antibodies.
Received: 28 April 1997 / Accepted: 24 June 1997 相似文献
54.
55.
Microarray-based comparative genomic analyses of the human malaria parasite Plasmodium falciparum using Affymetrix arrays 总被引:1,自引:0,他引:1
Carret CK Horrocks P Konfortov B Winzeler E Qureshi M Newbold C Ivens A 《Molecular and biochemical parasitology》2005,144(2):177-186
Microarray-based comparative genomic hybridization (CGH) provides a powerful tool for whole genome analyses and the rapid detection of genomic variation that underlies virulence and disease. In the field of Plasmodium research, many of the parasite genomes that one might wish to study in a high throughput manner are not laboratory clones, but clinical isolates. One of the key limitations to the use of clinical samples in CGH, however, is the miniscule amounts of genomic DNA available. Here we describe the successful application of multiple displacement amplification (MDA), a non-PCR-based amplification method that exhibits clear advantages over all other currently available methods. Using MDA, CGH was performed on a panel of NF54 and IT/FCR3 clones, identifying previously published deletions on chromosomes 2 and 9 as well as polymorphism in genes associated with disease pathology. 相似文献
56.
Graaff Esther de; Rouillard Patricia; J.Willems Patrick; P.T.Smits Arie; Rousseau Francois; A.Oostra Ben 《Human molecular genetics》1995,4(1):45-49
The fragile X syndrome is the most frequent cause of inheritedmental retardation. The molecular mechanism of the disorderis based on the expansion of a CGG repeat in the 5' UTR of theFMR1 gene In the majority of fragile X patients. The instabilityof this CGG repeat containing region is not restricted to theCGG repeat Itself but expands to the flanking region as well.We describe four unrelated fragile X patients that are mosaicfor both a full mutation and a small deletion in the CGG repeatcontaining region. Sequence analysis of the regions surroundingthe deletions showed that both the (CGG)n repeat and some flankingsequences were missing in all four patients. The 5' breakpointsof the deletions were found to be located between 7553bp proximal to the CGG repeat. This suggests the presence ofa hot spot region for deletions in the CGG repeat region ofthe FMR1 gene and emphasizes the instability of this regionIn the presence of an expanded CGG repeat. 相似文献
57.
The development of an M antibody capture ELISA for rubella IgM 总被引:2,自引:0,他引:2
An M antibody capture enzyme-linked immunosorbent assay for rubella IgM was developed. The enzyme label was prepared from a monoclonal antibody raised against rubella haemagglutinin (Tedder et al., 1982). Paired sera from acute rubella infections and vaccines as well as sera from blood donors, antenatal patients and patients whose sera contained rheumatoid factor and patients with acute non-rubella infections were tested by this method. 相似文献
58.
Selection in blood cells from female carriers of the fragile X syndrome: inverse correlation between age and proportion of active X chromosomes carrying the full mutation. 总被引:9,自引:3,他引:9
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We have studied the patterns of mutation and X inactivation in female carriers of a fragile X mutation, to try to correlate them with various phenotypic features. We used a simple assay, which shows simultaneously the size of the mutation, its methylation status, and DNA fragments that represent the normal active and inactive X chromosomes. We have observed an age dependent process, whereby the 'full' fragile X mutation is found preferentially on the inactive X in leucocytes in adult females, but not in younger ones. This phenomenon was not observed in female carriers of a 'premutation', who have little phenotypic expression. Preliminary data suggest that young females who show preferential presence of a full mutation on the active X in leucocytes may be at increased risk for mental retardation. We have also obtained preliminary evidence for an age dependent decrease in the somatic heterogeneity of full mutations, possibly owing to selection for smaller mutated fragments. If confirmed, the latter phenomenon might account for the known decrease with age of the expression of the fragile site. Our observations suggest that a gene whose expression is affected by the presence of a full mutation (possibly the FMR-1 gene) has a cell autonomous function in leucocytes, leading to a slowly progressive selection for cells where the mutation is on the inactive X chromosome. 相似文献
59.
Jehane Fadlallah Delphine Sterlin Claire Fieschi Christophe Parizot Karim Dorgham Hela El Kafsi Gaëlle Autaa Pascale Ghillani-Dalbin Catherine Juste Patricia Lepage Marion Malphettes Lionel Galicier David Boutboul Karine Clément Sébastien André Florian Marquet Christophe Tresallet Alexis Mathian Guy Gorochov 《The Journal of allergy and clinical immunology》2019,143(4):1575-1585.e4
60.
Maya?Ghoussaini David?Meyre Stéphane?Lobbens Guillaume?Charpentier Karine?Clément Marie-Aline?Charles Ma?té?Tauber Jacques?Weill Philippe?FroguelEmail author 《BMC medical genetics》2005,6(1):11