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81.
Regina Raz Kam Cheung Leona Ling David E. Levy 《Somatic Cell and Molecular Genetics》1995,21(2):139-145
The species specificity of interferons (IFNs) depends on restricted recognition of these ligands by multisubunit cell surface receptors. Expression of the human receptor subunit IFNAR in mouse cells conferred sensitivity only to one subtype of human IFN, IFN-B. Other genes on human chromosome 21 were required for responses to other subtypes of type I IFN. In contrast, IFNAR expression in hamster cells did not confer sensitivity to any human IFN tested, including IFN-B. Using human-hamster somatic cell hybrids, we mapped theIfnabr gene, encoding a ligand-binding subunit of the IFN-/ (type I) receptor, to human chromosome 21.Ifnabr colocalized withIfnar to the distal region of q22.1. The presence of a chromosomal fragment encoding IFNABR and IFNAR was also not sufficient to confer sensitivity to human IFN. In contrast, hybrids carrying in addition the region 21q22.2 showed a full response to human IFN-B, suggesting that a gene located in this region encodes a third factor required for type I IFN receptor activity. 相似文献
82.
Wong WW Doyle TC Cheung P Olson TM Reisler E 《Journal of muscle research and cell motility》2001,22(8):665-674
The molecular mechanisms by which different mutations in actin lead to distinct cardiomyopathies are unknown. Here, actin
mutants corresponding to α-cardiac actin mutations causing hypertrophic cardiomyopathy [(HCM) P164A and A331P] and dilated
cardiomyopathy [(DCM) R312H and E361G] were expressed in yeast and purified for in vitro functional studies. While P164A appeared unaltered compared to wild-type (WT) actin, A331P function was impaired. A331P showed
reduced stability in circular dichroism melting experiments; its monomer unfolding transition was 10°C lower compared to WT
actin. Additionally, in vitro filament formation was hampered, and yeast cell cultures were temperature sensitive, implying perturbations in actin–actin
interactions. Filament instability of the A331P mutant actin could lead to actomyosin dysfunction observed in HCM. Yeast strains
harboring the R312H mutation did not grow well in culture, suggesting that cell viability is compromised. The E361G substitution
is located at an α-actinin binding region where the actin filament is anchored. The mutant actin, though unaltered in the
in vitro motility and standard actomyosin functions, had a threefold reduction in α-actinin binding. This could result in impairment
of force-transduction in muscle fibers, and a DCM phenotype.
This revised version was published online in July 2006 with corrections to the Cover Date. 相似文献
83.
Evaluation of quantitative PCR and branched-chain DNA assay for detection of hepatitis B virus DNA in sera from hepatocellular carcinoma and liver transplant patients 总被引:4,自引:0,他引:4
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This study evaluated the applicability of quantitative PCR (Q-PCR) and branched-chain DNA assays for detection of hepatitis B virus (HBV) DNA in sera. For 42 samples, the detection rates were 81 and 41%, respectively, with a correlation coefficient of 0.633. The Q-PCR is useful for early monitoring of HBV load in high-risk patients. 相似文献
84.
Tang NL Hui J Law LK Lam YY Chan KY Yeung WL Chan AY Cheung KL Fok TF 《Human mutation》2000,16(5):446
Glutaric acidemia type I is caused by mutations of the glutaryl-CoA dehydrogenase (GCDH) gene resulting in loss of GCDH enzyme activity. Patients present with progressive dystonia and lesions in basal ganglia. Dietary treatment, when instituted from the early neonatal period, markedly reduces dystonia and morbidity. Early diagnosis and prenatal diagnosis will be facilitated by knowledge of locally prevalent GCDH mutations. Several common GCDH mutations have been found in different ethnic groups. GCDH mutations were studied in 5 Chinese glutaric acidemia type I families. We detected two novel recurrent mutations (A219T and IVS10-2A>C) which were found in two unrelated families. An asymptomatic carrier of IVS10-2A>C was also found on screening of 120 individuals. Other mutations were identified, including two other novel (R386G & IVS3+1G>A) and two known mutations (G178R & R355H). Fibroblasts from patients carrying the novel mutations were confirmed to be deficient for GCDH activity. This is the first report of GCDH mutations describing recurrent mutations in Chinese patients. The carrier rate of IVS10-2A>C may be particularly high in Chinese. 相似文献
85.
Chloe Miu Mak Ching-Wan Lam Sidney Tam Ching-Lung Lai Lik-Yuen Chan Sheung-Tat Fan Yu-Lung Lau Sik-To Lai Patrick Yuen Joannie Hui Chun-Cheung Fu Ka-Sing Wong Wing-Lai Mak Kong Tze Sui-Fan Tong Abby Lau Nancy Leung Aric Hui Ka-Ming Cheung Chun-Hung Ko Yiu-Ki Chan Oliver Ma Tai-Nin Chau Alexander Chiu Yan-Wo Chan 《Journal of human genetics》2008,53(4):375-375
86.
87.
88.
Detection and deletion of motion artifacts in electrogastrogram using feature analysis and neural networks 总被引:6,自引:0,他引:6
Electrogastrogram is a surface measurement of gastric myoelectrical activity, and electrogastrography has been an attractive
method for physiological and pathophysiological studies of the stomach due to its nonivasive nature. Motion artifacts, however,
ruin the electrogastrogram (EGG), and make the analysis very difficult and sometimes even impossible. They must be eliminated
from EGG signals before analysis. Up to now, this can only be done by visual inspection, which is not only time-consuming
but also subjective. In this study, a method using feature analysis and neural networks has been developed to realize automatic
detection and elimination of the motion artifacts in EGG recordings by computer. Experiments were conducted to investigate
the characteristics of different motion artifacts. Useful features were extracted, and different combinations of the features
used as the input of the neural network were compared to obtain the optimal performance for the detection of motion artifacts
using the artificial neural network. 相似文献
89.
90.
Distribution of mutations in the PEX gene in families with X-linked hypophosphataemic rickets (HYP) 总被引:8,自引:0,他引:8
Rowe PS; Oudet CL; Francis F; Sinding C; Pannetier S; Econs MJ; Strom TM; Meitinger T; Garabedian M; David A; Macher MA; Questiaux E; Popowska E; Pronicka E; Read AP; Mokrzycki A; Glorieux FH; Drezner MK; Hanauer A; Lehrach H; Goulding JN; O'Riordan JL 《Human molecular genetics》1997,6(4):539-549
Mutations in the PEX gene at Xp22.1 (phosphate-regulating gene with
homologies to endopeptidases, on the X-chromosome), are responsible for
X-linked hypophosphataemic rickets (HYP). Homology of PEX to the M13 family
of Zn2+ metallopeptidases which include neprilysin (NEP) as prototype, has
raised important questions regarding PEX function at the molecular level.
The aim of this study was to analyse 99 HYP families for PEX gene
mutations, and to correlate predicted changes in the protein structure with
Zn2+ metallopeptidase gene function. Primers flanking 22 characterised
exons were used to amplify DNA by PCR, and SSCP was then used to screen for
mutations. Deletions, insertions, nonsense mutations, stop codons and
splice mutations occurred in 83% of families screened for in all 22 exons,
and 51% of a separate set of families screened in 17 PEX gene exons.
Missense mutations in four regions of the gene were informative regarding
function, with one mutation in the Zn2+-binding site predicted to alter
substrate enzyme interaction and catalysis. Computer analysis of the
remaining mutations predicted changes in secondary structure,
N-glycosylation, protein phosphorylation and catalytic site molecular
structure. The wide range of mutations that align with regions required for
protease activity in NEP suggests that PEX also functions as a protease,
and may act by processing factor(s) involved in bone mineral metabolism.
相似文献