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801.
802.
803.
L. A. García-Alonso 《Cellular and molecular life sciences : CMLS》1999,55(11):1386-1398
The peripheral sensory system of the Drosophila adult has been used for the genetic analysis of axon guidance because of its accessibility for experimental manipulation
and mutant screens. Wing, leg, antenna, or eye sensory axons are able to pathfind normally under different perturbations,
indicating that sensory axon guidance is a highly canalized process. Similarly to other model systems, sensory growth cones
seem to use multiple, simultaneous cues for guidance. In addition, sensory axons from peripheral structures seem to be capable
of using alternative substrates for pathfinding. Developmental regulation could account for the high stability of axon guidance
under experimental and natural perturbation conditions. Despite this flexibility, functional characterization of genes involved
in sensory axon guidance is being carried out in situations where there appears to be less system redundancy. 相似文献
804.
Sinclair DA 《Cellular and molecular life sciences : CMLS》1999,56(9-10):807-816
The molecular mechanisms of aging are most fully understood for the budding yeast Saccharomyces cerevisiae. Recent advances in our understanding of aging in this organism have enabled researchers to answer some fundamental questions about the aging process. Is aging due to a multitude of 'mechanisms' or can there be a key few? Can we design single-gene mutations that will prolong life? Can we prolong life whilst maintaining health and fecundity? The various contributing factors to yeast longevity, uncovered thus far, fall into three classes: DNA metabolism, heterochromatin, and metabolic activity. However, these separate classes may actually represent different aspects of the same aging mechanism based on genome stability. This review examines the recent advances in our understanding of yeast aging and discusses their relevance, if any, to the human condition. 相似文献
805.
The Pendred syndrome gene encodes a chloride-iodide transport protein 总被引:24,自引:0,他引:24
Pendred syndrome is the most common form of syndromic deafness and characterized by congenital sensorineural hearing loss and goitre. This disorder was mapped to chromosome 7 and the gene causing Pendred syndrome (PDS) was subsequently identified by positional cloning. PDS encodes a putative transmembrane protein designated pendrin. Pendrin is closely related to a family of sulfate transport proteins that includes the rat sulfate-anion transporter (encoded by Sat-1; 29% amino acid sequence identity), the human diastrophic dysplasia sulfate transporter (encoded by DTD; 32%) and the human sulfate transporter 'downregulated in adenoma' (encoded by DRA; 45%). On the basis of this homology and the presence of a slightly modified sulfate-transporter signature sequence comprising its putative second transmembrane domain, pendrin has been proposed to function as a sulfate transporter. We were unable to detect evidence of sulfate transport following the expression of pendrin in Xenopus laevis oocytes by microinjection of PDS cRNA or in Sf9 cells following infection with PDS-recombinant baculovirus. The rates of transport for iodide and chloride were significantly increased following the expression of pendrin in both cell systems. Our results demonstrate that pendrin functions as a transporter of chloride and iodide, but not sulfate, and may provide insight into thyroid physiology and the pathophysiology of Pendred syndrome. 相似文献
806.
807.
Porcelli AM Ghelli A Mastrocola T Rugolo M 《Cellular and molecular life sciences : CMLS》1999,56(1-2):167-173
The Ca2+ ionophore ionomycin induced cytosolic [Ca2+]i elevation as well as strong activation of Cl− efflux in mouse mammary epithelial cell lines expressing wild-type or mutated (deletion of phenylalaline 508) cystic fibrosis
transmembrane conductance regulator (CFTR) or vector. Ionomycin-induced Cl− efflux was abolished by the intracellular Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid, whereas both activators and inhibitors of phospholipase A2 had no effect, indicating the involvement of Ca2+-dependent Cl- channels. Stimulation of arachidonic acid release by ionomycin and phorbol ester was not significantly different between
wild-type or mutated cell lines, whereas vector-transfected cells exhibited a significant higher release, which was shown
to be due to larger amount of immunoreactive cytosolic phospholipase A2. These results indicate that phospholipase A2 activity of C127 cells was not influenced by the presence of wild-type or mutated CFTR.
Received 27 April 1999; received after revision 11 June 1999; accepted 23 July 1999 相似文献
808.
Genomic instability in Gadd45a-deficient mice. 总被引:19,自引:0,他引:19
M C Hollander M S Sheikh D V Bulavin K Lundgren L Augeri-Henmueller R Shehee T A Molinaro K E Kim E Tolosa J D Ashwell M P Rosenberg Q Zhan P M Fernández-Salguero W F Morgan C X Deng A J Fornace 《Nature genetics》1999,23(2):176-184
Gadd45a-null mice generated by gene targeting exhibited several of the phenotypes characteristic of p53-deficient mice, including genomic instability, increased radiation carcinogenesis and a low frequency of exencephaly. Genomic instability was exemplified by aneuploidy, chromosome aberrations, gene amplification and centrosome amplification, and was accompanied by abnormalities in mitosis, cytokinesis and growth control. Unequal segregation of chromosomes due to multiple spindle poles during mitosis occurred in several Gadd45a -/- cell lineages and may contribute to the aneuploidy. Our results indicate that Gadd45a is one component of the p53 pathway that contributes to the maintenance of genomic stability. 相似文献
809.
810.
Engineering a mouse balancer chromosome. 总被引:15,自引:0,他引:15
B Zheng M Sage W W Cai D M Thompson B C Tavsanli Y C Cheah A Bradley 《Nature genetics》1999,22(4):375-378
Balancer chromosomes are genetic reagents that are used in Drosophila melanogaster for stock maintenance and mutagenesis screens. Despite their utility, balancer chromosomes are rarely used in mice because they are difficult to generate using conventional methods. Here we describe the engineering of a mouse balancer chromosome with the Cre-loxP recombination system. The chromosome features a 24-centiMorgan (cM) inversion between Trp53 (also known as p53) and Wnt3 on mouse chromosome 11 that is recessive lethal and dominantly marked with a K14-Agouti transgene. When allelic to a wild-type chromosome, the inversion suppresses crossing over in the inversion interval, accompanied by elevated recombination in the flanking regions. The inversion functions as a balancer chromosome because it can be used to maintain a lethal mutation in the inversion interval as a self-sustaining trans-heterozygous stock. This strategy can be used to generate similar genetic reagents throughout the mouse genome. Engineering of visibly marked inversions and deficiencies is an important step toward functional analyses of the mouse genome and will facilitate large-scale mutagenesis programs. 相似文献