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排序方式: 共有2157条查询结果,搜索用时 15 毫秒
961.
HIV-CAUSAL Collaboration Cain LE Logan R Robins JM Sterne JA Sabin C Bansi L Justice A Goulet J van Sighem A de Wolf F Bucher HC von Wyl V Esteve A Casabona J del Amo J Moreno S Seng R Meyer L Perez-Hoyos S Muga R Lodi S Lanoy E Costagliola D Hernan MA 《Annals of internal medicine》2011,154(8):509-515
962.
The EMT regulator Zeb2/Sip1 is essential for murine embryonic hematopoietic stem/progenitor cell differentiation and mobilization 总被引:1,自引:0,他引:1
963.
964.
Mateo M Carbonnelle C Reynard O Kolesnikova L Nemirov K Page A Volchkova VA Volchkov VE 《The Journal of infectious diseases》2011,204(Z3):S1011-S1020
In sharp contrast to human and nonhuman primates, guinea pigs and some other mammals resist Ebola virus (EBOV) replication and do not develop illness upon virus inoculation. However, serial passaging of EBOV in guinea pigs results in a selection of variants with high pathogenicity. In this report, using a reverse genetics approach, we demonstrate that this dramatic increase in EBOV pathogenicity is associated with amino acid substitutions in the structural protein VP24. We show that although replication of recombinant EBOV carrying wild-type VP24 is impaired in primary peritoneal guinea pig macrophages and in the liver of infected animals, the substitutions in VP24 allow EBOV to replicate in guinea pig macrophages and spread in the liver of infected animals. Furthermore, we demonstrate that both VP24/wild type and the guinea pig-adapted VP24/8mc are similar in their ability to block expression of interferon-induced host genes, suggesting that the increase in EBOV virulence for guinea pigs is not associated with VP24 interferon antagonist function. This study sheds light on the mechanism of resistance to EBOV infection and highlights the critical role of VP24 in EBOV pathogenesis. 相似文献
965.
Jana Kopecká Jakub Krijt Kateřina Raková Viktor Kožich 《Journal of inherited metabolic disease》2011,34(1):39-48
Misfolding and aggregation of mutant enzymes have been proposed to play role in the pathogenesis of homocystinuria due to
cystathionine β-synthase (CBS) deficiency. Chemical chaperones have been recently shown to facilitate proper assembly of several
CBS mutants. To asses the number of patients that may respond to chaperone therapy, we examined the effect of selected CBS
ligands and osmolytes on assembly and activity of 27 CBS mutants that represent 70% of known CBS alleles. The mutant enzymes
were expressed in a bacterial system, and their properties were assessed by native Western blotting and sensitive liquid chromatography
tandem mass spectrometry (LC-MS/MS) assay, respectively. We studied the chaperoning activity of δ-aminolevulinic acid (δ-ALA)—a
heme precursor—and of three osmolytes betaine, 2-aminoethanesulfonic acid (taurine), and glycerol. Fourteen mutants responded
by at least 30% increase in the amount of correctly assembled tetramers and enzymatic activity to the coexpressional presence
of either 0.5 mM δ-ALA, 100 mM betaine, and/or 750 mM glycerol. Eight of these mutants (p.R266K, p.P49L, p.R125Q, p.K102N,
p.R369C, p.V180A, p.P78R, p.S466L) were rescuable by all of these three substances. Four mutants showed increased formation
of tetramers that was not accompanied by changes in activity. Topology of mutations appeared to determine the chaperone responsiveness,
as 11 of 14 solvent-exposed mutations were substantially more responsive than three of 13 buried mutations. This study identified
chaperone-responsive mutants that represent 56 of 713 known patient-derived CBS alleles and may serve as a basis for exploring
pharmacological approaches aimed at correcting misfolding in homocystinuria. 相似文献
966.
Haxhihamza K Doarn CR Marija R Dimitrinka JP Rozalinda I Izabela F Viktor I Lidija S 《Telemedicine journal and e-health》2011,17(9):700-704
Domestic and peer violence in Macedonia is similar to other developed nations. It is present among adolescents and their families. A study was conducted on 664 secondary school students throughout Macedonia. The results indicated that 11.2% male and 16.54% female students often face different kinds of family violence. Peer violence of different forms is marked as "often" in 8.04% male respondents and 5.63% female respondents. One of possibilities in preventing this negative phenomenon is the application of telemedicine. There is a growing body of evidence that the use of telemedicine offers a good tool for mental healthcare in underserved communities, and that these services are as effective as face-to-face work with adolescents. By building an effective telemedicine network in Macedonia, both victims (adolescents) and their parents could be given a chance to contact proper institutions for help with more confidence and less stress. 相似文献
967.
968.
Liu L Okada S Kong XF Kreins AY Cypowyj S Abhyankar A Toubiana J Itan Y Audry M Nitschke P Masson C Toth B Flatot J Migaud M Chrabieh M Kochetkov T Bolze A Borghesi A Toulon A Hiller J Eyerich S Eyerich K Gulácsy V Chernyshova L Chernyshov V Bondarenko A Grimaldo RM Blancas-Galicia L Beas IM Roesler J Magdorf K Engelhard D Thumerelle C Burgel PR Hoernes M Drexel B Seger R Kusuma T Jansson AF Sawalle-Belohradsky J Belohradsky B Jouanguy E Bustamante J Bué M Karin N Wildbaum G Bodemer C 《The Journal of experimental medicine》2011,208(8):1635-1648
Chronic mucocutaneous candidiasis disease (CMCD) may be caused by autosomal dominant (AD) IL-17F deficiency or autosomal recessive (AR) IL-17RA deficiency. Here, using whole-exome sequencing, we identified heterozygous germline mutations in STAT1 in 47 patients from 20 kindreds with AD CMCD. Previously described heterozygous STAT1 mutant alleles are loss-of-function and cause AD predisposition to mycobacterial disease caused by impaired STAT1-dependent cellular responses to IFN-γ. Other loss-of-function STAT1 alleles cause AR predisposition to intracellular bacterial and viral diseases, caused by impaired STAT1-dependent responses to IFN-α/β, IFN-γ, IFN-λ, and IL-27. In contrast, the 12 AD CMCD-inducing STAT1 mutant alleles described here are gain-of-function and increase STAT1-dependent cellular responses to these cytokines, and to cytokines that predominantly activate STAT3, such as IL-6 and IL-21. All of these mutations affect the coiled-coil domain and impair the nuclear dephosphorylation of activated STAT1, accounting for their gain-of-function and dominance. Stronger cellular responses to the STAT1-dependent IL-17 inhibitors IFN-α/β, IFN-γ, and IL-27, and stronger STAT1 activation in response to the STAT3-dependent IL-17 inducers IL-6 and IL-21, hinder the development of T cells producing IL-17A, IL-17F, and IL-22. Gain-of-function STAT1 alleles therefore cause AD CMCD by impairing IL-17 immunity. 相似文献
969.
The phage typing of 3900 isolates of Salmonella Enteritidis and 1741 isolates of Salmonella Typhimurium has been carried out in the period 1995-2009. Among Salmonella Enteritidis in individual years, the most prevalent phage type (PT) was 8. The most predominant PTs of Salmonella Typhimurium were DT104 and U302. 相似文献
970.