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排序方式: 共有388条查询结果,搜索用时 31 毫秒
181.
Didier Fraix-Burnet Philippe Choler Emmanuel J.P. Douzery Anne Verhamme 《Journal of Classification》2006,23(1):31-56
This series of papers is intended to present astrocladistics in some detail and evaluate this methodology in reconstructing
phylogenies of galaxies. Being based on the evolution of all the characters describing galaxies, it is an objective way of
understanding galaxy diversity through evolutionary relationships. In this first paper, we present the basic steps of a cladistic
analysis and show both theoretically and practically that it can be applied to galaxies. For illustration, we use a sample
of 50 simulated galaxies taken from the GALICS database, which are described by 91 observables (dynamics, masses and luminosities).
These 50 simulated galaxies are indeed 10 different galaxies taken at 5 cosmological epochs, and they are free of merger events.
The astrocladistic analysis easily reconstructs the true chronology of evolution relationships within this sample. It also
demonstrates that burst characters are not relevant for galaxy evolution as a whole. A companion paper is devoted to the formalization
of the concepts of formation and diversification in galaxy evolution. 相似文献
182.
N O Bianchi 《Experientia》1973,29(10):1301-1302
183.
The ELF4-ELF3-LUX complex links the circadian clock to diurnal control of hypocotyl growth 总被引:1,自引:0,他引:1
Nusinow DA Helfer A Hamilton EE King JJ Imaizumi T Schultz TF Farré EM Kay SA 《Nature》2011,475(7356):398-402
184.
Yokoyama S Woods SL Boyle GM Aoude LG MacGregor S Zismann V Gartside M Cust AE Haq R Harland M Taylor JC Duffy DL Holohan K Dutton-Regester K Palmer JM Bonazzi V Stark MS Symmons J Law MH Schmidt C Lanagan C O'Connor L Holland EA Schmid H Maskiell JA Jetann J Ferguson M Jenkins MA Kefford RF Giles GG Armstrong BK Aitken JF Hopper JL Whiteman DC Pharoah PD Easton DF Dunning AM Newton-Bishop JA Montgomery GW Martin NG Mann GJ Bishop DT Tsao H Trent JM Fisher DE Hayward NK Brown KM 《Nature》2011,480(7375):99-103
185.
Schreiber A Stengel F Zhang Z Enchev RI Kong EH Morris EP Robinson CV da Fonseca PC Barford D 《Nature》2011,470(7333):227-232
The anaphase-promoting complex or cyclosome (APC/C) is an unusually large E3 ubiquitin ligase responsible for regulating defined cell cycle transitions. Information on how its 13 constituent proteins are assembled, and how they interact with co-activators, substrates and regulatory proteins is limited. Here, we describe a recombinant expression system that allows the reconstitution of holo APC/C and its sub-complexes that, when combined with electron microscopy, mass spectrometry and docking of crystallographic and homology-derived coordinates, provides a precise definition of the organization and structure of all essential APC/C subunits, resulting in a pseudo-atomic model for 70% of the APC/C. A lattice-like appearance of the APC/C is generated by multiple repeat motifs of most APC/C subunits. Three conserved tetratricopeptide repeat (TPR) subunits (Cdc16, Cdc23 and Cdc27) share related superhelical homo-dimeric architectures that assemble to generate a quasi-symmetrical structure. Our structure explains how this TPR sub-complex, together with additional scaffolding subunits (Apc1, Apc4 and Apc5), coordinate the juxtaposition of the catalytic and substrate recognition module (Apc2, Apc11 and Apc10 (also known as Doc1)), and TPR-phosphorylation sites, relative to co-activator, regulatory proteins and substrates. 相似文献
186.
In Drosophila, four genes encode for laminin subunits and the formation of two laminin heterotrimers has been postulated. We report the
identification of mutations in the Drosophila LamininB2 (LanB2) gene that encodes for the only laminin γ subunit and is found in both heterotrimers. We describe their effects on embryogenesis,
in particular the differentiation of visceral tissues with respect to the ECM. Analysis of mesoderm endoderm interaction indicates
disrupted basement membranes and defective endoderm migration, which finally interferes with visceral myotube stretching.
Extracellular deposition of laminin is blocked due to the loss of the LanB2 subunit, resulting in an abnormal distribution
of ECM components. Our data, concerning the different function of both trimers during organogenesis, suggest that these trimers
might act in a cumulative way and probably at multiple steps during ECM assembly. We also observed genetic interactions with
kon-tiki and thrombospondin, indicating a role for laminin during muscle attachment. 相似文献
187.
Jann E. Vendetti Emily Burnett Lidia Carlton Anne T. Curran Cedric Lee Ron Matsumoto 《Journal of Natural History》2019,53(25-26):1607-1632
188.
Lene Buhl-Mortensen Anne Helene S. Tandberg Pål Buhl-Mortensen Andrew R. Gates 《Journal of Natural History》2016,50(5-6):323-337
There are few in situ observations of deep-sea macrofauna, due to the remoteness of this ecosystem. Visual surveys conducted for marine management by MAREANO, (marine area database for Norwegian waters) and the petroleum industry (by SERPENTS, scientific and environmental remotely operated vehicle partnership using existing industrial technology) have provided unique material of visual information from large areas in the Norwegian Sea. The distribution, density and behaviour of the deep-sea amphipod Neohela monstrosa (Boeck, 1861) is described based on videos and samples from the Norwegian Sea. This amphipod is common on mud bottoms at 200–2181 m depth in the area. Dense communities were found in stands of the arctic sea pen Umbellula encrinus at more than 1000 m depth where temperatures were below 0° C. The mean density of N. monstrosa observed for larger areas was 4/100 m2 but densities of 15–36 individuals per m2 were found in local patches. It is domicolous which is characteristic of the superfamily Corophiida and digs burrows in soft muddy bottoms primarily by using large shovel-like gnathopods to scoop the sediment out. The amphipod was observed pushing and rolling sediment balls out of its burrow, which were probably held together with amphipod silk. It digs out an upper 3 to 4 cm wide burrow with a horizontal side burrow a couple of centimetres down. Neohela monstrosa appears to feeds on newly settled detritus that it collects from the surface sediment through the use of its long antennae while the burrow is mainly used for protection against predators such as demersal fish. Newly released juveniles are probably kept in the burrow for protection. Based on the local high density of N. monstrosa together with its habit of making long burrows, we suggest that there is significant bioturbation associated with the presence of N. monstrosa in deep sedimentary habitats of the Norwegian Sea, which likely provides an important ecosystem function. 相似文献
189.
Hundreds of variants clustered in genomic loci and biological pathways affect human height 总被引:2,自引:0,他引:2
Lango Allen H Estrada K Lettre G Berndt SI Weedon MN Rivadeneira F Willer CJ Jackson AU Vedantam S Raychaudhuri S Ferreira T Wood AR Weyant RJ Segrè AV Speliotes EK Wheeler E Soranzo N Park JH Yang J Gudbjartsson D Heard-Costa NL Randall JC Qi L Vernon Smith A Mägi R Pastinen T Liang L Heid IM Luan J Thorleifsson G Winkler TW Goddard ME Sin Lo K Palmer C Workalemahu T Aulchenko YS Johansson A Zillikens MC Feitosa MF Esko T Johnson T Ketkar S Kraft P Mangino M Prokopenko I Absher D Albrecht E 《Nature》2010,467(7317):832-838
Most common human traits and diseases have a polygenic pattern of inheritance: DNA sequence variants at many genetic loci influence the phenotype. Genome-wide association (GWA) studies have identified more than 600 variants associated with human traits, but these typically explain small fractions of phenotypic variation, raising questions about the use of further studies. Here, using 183,727 individuals, we show that hundreds of genetic variants, in at least 180 loci, influence adult height, a highly heritable and classic polygenic trait. The large number of loci reveals patterns with important implications for genetic studies of common human diseases and traits. First, the 180 loci are not random, but instead are enriched for genes that are connected in biological pathways (P = 0.016) and that underlie skeletal growth defects (P?0.001). Second, the likely causal gene is often located near the most strongly associated variant: in 13 of 21 loci containing a known skeletal growth gene, that gene was closest to the associated variant. Third, at least 19 loci have multiple independently associated variants, suggesting that allelic heterogeneity is a frequent feature of polygenic traits, that comprehensive explorations of already-discovered loci should discover additional variants and that an appreciable fraction of associated loci may have been identified. Fourth, associated variants are enriched for likely functional effects on genes, being over-represented among variants that alter amino-acid structure of proteins and expression levels of nearby genes. Our data explain approximately 10% of the phenotypic variation in height, and we estimate that unidentified common variants of similar effect sizes would increase this figure to approximately 16% of phenotypic variation (approximately 20% of heritable variation). Although additional approaches are needed to dissect the genetic architecture of polygenic human traits fully, our findings indicate that GWA studies can identify large numbers of loci that implicate biologically relevant genes and pathways. 相似文献
190.
Probing sporadic and familial Alzheimer's disease using induced pluripotent stem cells 总被引:1,自引:0,他引:1
Israel MA Yuan SH Bardy C Reyna SM Mu Y Herrera C Hefferan MP Van Gorp S Nazor KL Boscolo FS Carson CT Laurent LC Marsala M Gage FH Remes AM Koo EH Goldstein LS 《Nature》2012,482(7384):216-220
Our understanding of Alzheimer's disease pathogenesis is currently limited by difficulties in obtaining live neurons from patients and the inability to model the sporadic form of the disease. It may be possible to overcome these challenges by reprogramming primary cells from patients into induced pluripotent stem cells (iPSCs). Here we reprogrammed primary fibroblasts from two patients with familial Alzheimer's disease, both caused by a duplication of the amyloid-β precursor protein gene (APP; termed APP(Dp)), two with sporadic Alzheimer's disease (termed sAD1, sAD2) and two non-demented control individuals into iPSC lines. Neurons from differentiated cultures were purified with fluorescence-activated cell sorting and characterized. Purified cultures contained more than 90% neurons, clustered with fetal brain messenger RNA samples by microarray criteria, and could form functional synaptic contacts. Virtually all cells exhibited normal electrophysiological activity. Relative to controls, iPSC-derived, purified neurons from the two APP(Dp) patients and patient sAD2 exhibited significantly higher levels of the pathological markers amyloid-β(1-40), phospho-tau(Thr?231) and active glycogen synthase kinase-3β (aGSK-3β). Neurons from APP(Dp) and sAD2 patients also accumulated large RAB5-positive early endosomes compared to controls. Treatment of purified neurons with β-secretase inhibitors, but not γ-secretase inhibitors, caused significant reductions in phospho-Tau(Thr?231) and aGSK-3β levels. These results suggest a direct relationship between APP proteolytic processing, but not amyloid-β, in GSK-3β activation and tau phosphorylation in human neurons. Additionally, we observed that neurons with the genome of one sAD patient exhibited the phenotypes seen in familial Alzheimer's disease samples. More generally, we demonstrate that iPSC technology can be used to observe phenotypes relevant to Alzheimer's disease, even though it can take decades for overt disease to manifest in patients. 相似文献