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181.
182.
C. H. Clarke 《Cellular and molecular life sciences : CMLS》1961,17(11):499-501
Résumé L'auteur décrit un mutant auxotrophe pour l'arginine chezSalmonella typhimurium. Les prototrophes arg+ sont induits par les rayons UV, MnCl2 et méthane sulfonate d'éthyle. Le-propiolactone est moins efficace pour l'induction des arg+. La transduction avec le bactériophage PLT-22 cultivé sur une souche prototrophe donne arg+ à une fréquence de 1/107 bactériophages. Le mutant arg– est fécond ni avec les souches d'Escherichia coli K-12 HfrC et HfrH ni avec trois souches deKlebsiella pneumoniae.
I am very grateful to Professor D. G.Catcheside, F.R.S., for his invaluable encouragement and advice, and to the Agricultural Research Council for the award of a Research Studentship. 相似文献
I am very grateful to Professor D. G.Catcheside, F.R.S., for his invaluable encouragement and advice, and to the Agricultural Research Council for the award of a Research Studentship. 相似文献
183.
Antoci V Handler G Campante TL Thygesen AO Moya A Kallinger T Stello D Grigahcène A Kjeldsen H Bedding TR Lüftinger T Christensen-Dalsgaard J Catanzaro G Frasca A De Cat P Uytterhoeven K Bruntt H Houdek G Kurtz DW Lenz P Kaiser A Van Cleve J Allen C Clarke BD 《Nature》2011,477(7366):570-573
Delta Scuti (δSct) stars are opacity-driven pulsators with masses of 1.5-2.5 M⊙, their pulsations resulting from the varying ionization of helium. In less massive stars such as the Sun, convection transports mass and energy through the outer 30 per cent of the star and excites a rich spectrum of resonant acoustic modes. Based on the solar example, with no firm theoretical basis, models predict that the convective envelope in δSct stars extends only about 1 per cent of the radius, but with sufficient energy to excite solar-like oscillations. This was not observed before the Kepler mission, so the presence of a convective envelope in the models has been questioned. Here we report the detection of solar-like oscillations in the δSct star HD187547, implying that surface convection operates efficiently in stars about twice as massive as the Sun, as the ad hoc models predicted. 相似文献
184.
Borgia MB Borgia A Best RB Steward A Nettels D Wunderlich B Schuler B Clarke J 《Nature》2011,474(7353):662-665
A large range of debilitating medical conditions is linked to protein misfolding, which may compete with productive folding particularly in proteins containing multiple domains. Seventy-five per cent of the eukaryotic proteome consists of multidomain proteins, yet it is not understood how interdomain misfolding is avoided. It has been proposed that maintaining low sequence identity between covalently linked domains is a mechanism to avoid misfolding. Here we use single-molecule F?rster resonance energy transfer to detect and quantify rare misfolding events in tandem immunoglobulin domains from the I band of titin under native conditions. About 5.5 per cent of molecules with identical domains misfold during refolding in vitro and form an unexpectedly stable state with an unfolding half-time of several days. Tandem arrays of immunoglobulin-like domains in humans show significantly lower sequence identity between neighbouring domains than between non-adjacent domains. In particular, the sequence identity of neighbouring domains has been found to be preferentially below 40 per cent. We observe no misfolding for a tandem of naturally neighbouring domains with low sequence identity (24 per cent), whereas misfolding occurs between domains that are 42 per cent identical. Coarse-grained molecular simulations predict the formation of domain-swapped structures that are in excellent agreement with the observed transfer efficiency of the misfolded species. We infer that the interactions underlying misfolding are very specific and result in a sequence-specific domain-swapping mechanism. Diversifying the sequence between neighbouring domains seems to be a successful evolutionary strategy to avoid misfolding in multidomain proteins. 相似文献
185.
Haematopoiesis is maintained by a hierarchical system where haematopoietic stem cells (HSCs) give rise to multipotent progenitors, which in turn differentiate into all types of mature blood cells. HSCs maintain themselves for the lifetime of the organism because of their ability to self-renew. However, multipotent progenitors lack the ability to self-renew, therefore their mitotic capacity and expansion potential are limited and they are destined to eventually stop proliferating after a finite number of cell divisions. The molecular mechanisms that limit the proliferation capacity of multipotent progenitors and other more mature progenitors are not fully understood. Here we show that bone marrow cells from mice deficient in three genes genetically downstream of Bmi1--p16Ink4a, p19Arf and Trp53 (triple mutant mice; p16Ink4a and p19Arf are alternative reading frames of the same gene (also called Cdkn2a) that encode different proteins)--have an approximately 10-fold increase in cells able to reconstitute the blood long term. This increase is associated with the acquisition of long-term reconstitution capacity by cells of the phenotype c-kit+Sca-1+Flt3+CD150-CD48-Lin-, which defines multipotent progenitors in wild-type mice. The pattern of triple mutant multipotent progenitor response to growth factors resembles that of wild-type multipotent progenitors but not wild-type HSCs. These results demonstrate that p16Ink4a/p19Arf and Trp53 have a central role in limiting the expansion potential of multipotent progenitors. These pathways are commonly repressed in cancer, suggesting a mechanism by which early progenitor cells could gain the ability to self-renew and become malignant with further oncogenic mutations. 相似文献
186.
Dong C Beis K Nesper J Brunkan-Lamontagne AL Clarke BR Whitfield C Naismith JH 《Nature》2006,444(7116):226-229
Many types of bacteria produce extracellular polysaccharides (EPSs). Some are secreted polymers and show only limited association with the cell surface, whereas others are firmly attached to the cell surface and form a discrete structural layer, the capsule, which envelopes the cell and allows the bacteria to evade or counteract the host immune system. EPSs have critical roles in bacterial colonization of surfaces, such as epithelia and medical implants; in addition some EPSs have important industrial and biomedical applications in their own right. Here we describe the 2.26 A resolution structure of the 340 kDa octamer of Wza, an integral outer membrane lipoprotein, which is essential for group 1 capsule export in Escherichia coli. The transmembrane region is a novel alpha-helical barrel. The bulk of the Wza structure is located in the periplasm and comprises three novel domains forming a large central cavity. Wza is open to the extracellular environment but closed to the periplasm. We propose a route and mechanism for translocation of the capsular polysaccharide. This work may provide insight into the export of other large polar molecules such as DNA and proteins. 相似文献
187.
A human IFNGR1 small deletion hotspot associated with dominant susceptibility to mycobacterial infection 总被引:25,自引:0,他引:25
Jouanguy E Lamhamedi-Cherradi S Lammas D Dorman SE Fondanèche MC Dupuis S Döffinger R Altare F Girdlestone J Emile JF Ducoulombier H Edgar D Clarke J Oxelius VA Brai M Novelli V Heyne K Fischer A Holland SM Kumararatne DS Schreiber RD Casanova JL 《Nature genetics》1999,21(4):370-378
The immunogenetic basis of severe infections caused by bacille Calmette-Guérin vaccine and environmental mycobacteria in humans remains largely unknown. We describe 18 patients from several generations of 12 unrelated families who were heterozygous for 1 to 5 overlapping IFNGR1 frameshift small deletions and a wild-type IFNGR1 allele. There were 12 independent mutation events at a single mutation site, defining a small deletion hotspot. Neighbouring sequence analysis favours a small deletion model of slipped mispairing events during replication. The mutant alleles encode cell-surface IFNgamma receptors that lack the intra-cytoplasmic domain, which, through a combination of impaired recycling, abrogated signalling and normal binding to IFNgamma exert a dominant-negative effect. We thus report a hotspot for human IFNGR1 small deletions that confer dominant susceptibility to infections caused by poorly virulent mycobacteria. 相似文献