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31.
Genome duplication in the teleost fish Tetraodon nigroviridis reveals the early vertebrate proto-karyotype 总被引:2,自引:0,他引:2
Jaillon O Aury JM Brunet F Petit JL Stange-Thomann N Mauceli E Bouneau L Fischer C Ozouf-Costaz C Bernot A Nicaud S Jaffe D Fisher S Lutfalla G Dossat C Segurens B Dasilva C Salanoubat M Levy M Boudet N Castellano S Anthouard V Jubin C Castelli V Katinka M Vacherie B Biémont C Skalli Z Cattolico L Poulain J De Berardinis V Cruaud C Duprat S Brottier P Coutanceau JP Gouzy J Parra G Lardier G Chapple C McKernan KJ McEwan P Bosak S Kellis M Volff JN Guigó R Zody MC Mesirov J Lindblad-Toh K 《Nature》2004,431(7011):946-957
Tetraodon nigroviridis is a freshwater puffer fish with the smallest known vertebrate genome. Here, we report a draft genome sequence with long-range linkage and substantial anchoring to the 21 Tetraodon chromosomes. Genome analysis provides a greatly improved fish gene catalogue, including identifying key genes previously thought to be absent in fish. Comparison with other vertebrates and a urochordate indicates that fish proteins have diverged markedly faster than their mammalian homologues. Comparison with the human genome suggests approximately 900 previously unannotated human genes. Analysis of the Tetraodon and human genomes shows that whole-genome duplication occurred in the teleost fish lineage, subsequent to its divergence from mammals. The analysis also makes it possible to infer the basic structure of the ancestral bony vertebrate genome, which was composed of 12 chromosomes, and to reconstruct much of the evolutionary history of ancient and recent chromosome rearrangements leading to the modern human karyotype. 相似文献
32.
Ron Levy 《Systemic Practice and Action Research》1991,4(2):87-99
In response to the call that systems practitioners need to produce a second epistemological break corresponding to a shift of interest from systems science to systems rationality, it is submitted that the preparation for this break has already been carried out. It is shown that systems rationality is firmly established and central to the French school of thought in systemics and that the philosophical groundwork has been extensively laid out by Edgar Morin. A very limited exposé of Morin's work is presented in support of this claim. 相似文献
33.
Bovee D Zhou Y Haugen E Wu Z Hayden HS Gillett W Tuzun E Cooper GM Sampas N Phelps K Levy R Morrison VA Sprague J Jewett D Buckley D Subramaniam S Chang J Smith DR Olson MV Eichler EE Kaul R 《Nature genetics》2008,40(1):96-101
The human genome sequence has been finished to very high standards; however, more than 340 gaps remained when the finished genome was published by the International Human Genome Sequencing Consortium in 2004. Using fosmid resources generated from multiple individuals, we targeted gaps in the euchromatic part of the human genome. Here we report 2,488,842 bp of previously unknown euchromatic sequence, 363,114 bp of which close 26 of 250 euchromatic gaps, or 10%, including two remaining euchromatic gaps on chromosome 19. Eight (30.7%) of the closed gaps were found to be polymorphic. These sequences allow complete annotation of several human genes as well as the assignment of mRNAs. The gap sequences are 2.3-fold enriched in segmentally duplicated sequences compared to the whole genome. Our analysis confirms that not all gaps within 'finished' genomes are recalcitrant to subcloning and suggests that the paired-end-sequenced fosmid libraries could prove to be a rich resource for completion of the human euchromatic genome. 相似文献
34.
Hereditary pancreatitis caused by triplication of the trypsinogen locus 总被引:12,自引:0,他引:12
Le Maréchal C Masson E Chen JM Morel F Ruszniewski P Levy P Férec C 《Nature genetics》2006,38(12):1372-1374
Hereditary pancreatitis has been reported to be caused by 'gain-of-function' missense mutations in the cationic trypsinogen gene (PRSS1). Here we report the triplication of a approximately 605-kb segment containing the PRSS1 gene on chromosome 7 in five families with hereditary pancreatitis. This triplication, which seems to result in a gain of trypsin through a gene dosage effect, represents a previously unknown molecular mechanism causing hereditary pancreatitis. 相似文献
35.
Radisky DC Levy DD Littlepage LE Liu H Nelson CM Fata JE Leake D Godden EL Albertson DG Nieto MA Werb Z Bissell MJ 《Nature》2005,436(7047):123-127
36.
Activation of the DNA damage checkpoint and genomic instability in human precancerous lesions 总被引:5,自引:0,他引:5
Gorgoulis VG Vassiliou LV Karakaidos P Zacharatos P Kotsinas A Liloglou T Venere M Ditullio RA Kastrinakis NG Levy B Kletsas D Yoneta A Herlyn M Kittas C Halazonetis TD 《Nature》2005,434(7035):907-913
DNA damage checkpoint genes, such as p53, are frequently mutated in human cancer, but the selective pressure for their inactivation remains elusive. We analysed a panel of human lung hyperplasias, all of which retained wild-type p53 genes and had no signs of gross chromosomal instability, and found signs of a DNA damage response, including histone H2AX and Chk2 phosphorylation, p53 accumulation, focal staining of p53 binding protein 1 (53BP1) and apoptosis. Progression to carcinoma was associated with p53 or 53BP1 inactivation and decreased apoptosis. A DNA damage response was also observed in dysplastic nevi and in human skin xenografts, in which hyperplasia was induced by overexpression of growth factors. Both lung and experimentally-induced skin hyperplasias showed allelic imbalance at loci that are prone to DNA double-strand break formation when DNA replication is compromised (common fragile sites). We propose that, from its earliest stages, cancer development is associated with DNA replication stress, which leads to DNA double-strand breaks, genomic instability and selective pressure for p53 mutations. 相似文献
37.
Distinct types of diffuse large B-cell lymphoma identified by gene expression profiling 总被引:366,自引:0,他引:366
Alizadeh AA Eisen MB Davis RE Ma C Lossos IS Rosenwald A Boldrick JC Sabet H Tran T Yu X Powell JI Yang L Marti GE Moore T Hudson J Lu L Lewis DB Tibshirani R Sherlock G Chan WC Greiner TC Weisenburger DD Armitage JO Warnke R Levy R Wilson W Grever MR Byrd JC Botstein D Brown PO Staudt LM 《Nature》2000,403(6769):503-511
Diffuse large B-cell lymphoma (DLBCL), the most common subtype of non-Hodgkin's lymphoma, is clinically heterogeneous: 40% of patients respond well to current therapy and have prolonged survival, whereas the remainder succumb to the disease. We proposed that this variability in natural history reflects unrecognized molecular heterogeneity in the tumours. Using DNA microarrays, we have conducted a systematic characterization of gene expression in B-cell malignancies. Here we show that there is diversity in gene expression among the tumours of DLBCL patients, apparently reflecting the variation in tumour proliferation rate, host response and differentiation state of the tumour. We identified two molecularly distinct forms of DLBCL which had gene expression patterns indicative of different stages of B-cell differentiation. One type expressed genes characteristic of germinal centre B cells ('germinal centre B-like DLBCL'); the second type expressed genes normally induced during in vitro activation of peripheral blood B cells ('activated B-like DLBCL'). Patients with germinal centre B-like DLBCL had a significantly better overall survival than those with activated B-like DLBCL. The molecular classification of tumours on the basis of gene expression can thus identify previously undetected and clinically significant subtypes of cancer. 相似文献
38.
Human serum beta lipoprotein and beta apoprotein 总被引:1,自引:0,他引:1
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