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121.
Optically healable supramolecular polymers 总被引:2,自引:0,他引:2
Burnworth M Tang L Kumpfer JR Duncan AJ Beyer FL Fiore GL Rowan SJ Weder C 《Nature》2011,472(7343):334-337
Polymers with the ability to repair themselves after sustaining damage could extend the lifetimes of materials used in many applications. Most approaches to healable materials require heating the damaged area. Here we present metallosupramolecular polymers that can be mended through exposure to light. They consist of telechelic, rubbery, low-molecular-mass polymers with ligand end groups that are non-covalently linked through metal-ion binding. On exposure to ultraviolet light, the metal-ligand motifs are electronically excited and the absorbed energy is converted into heat. This causes temporary disengagement of the metal-ligand motifs and a concomitant reversible decrease in the polymers' molecular mass and viscosity, thereby allowing quick and efficient defect healing. Light can be applied locally to a damage site, so objects can in principle be healed under load. We anticipate that this approach to healable materials, based on supramolecular polymers and a light-heat conversion step, can be applied to a wide range of supramolecular materials that use different chemistries. 相似文献
122.
Structure-based design of non-natural amino-acid inhibitors of amyloid fibril formation 总被引:2,自引:0,他引:2
Sievers SA Karanicolas J Chang HW Zhao A Jiang L Zirafi O Stevens JT Münch J Baker D Eisenberg D 《Nature》2011,475(7354):96-100
Many globular and natively disordered proteins can convert into amyloid fibrils. These fibrils are associated with numerous pathologies as well as with normal cellular functions, and frequently form during protein denaturation. Inhibitors of pathological amyloid fibril formation could be useful in the development of therapeutics, provided that the inhibitors were specific enough to avoid interfering with normal processes. Here we show that computer-aided, structure-based design can yield highly specific peptide inhibitors of amyloid formation. Using known atomic structures of segments of amyloid fibrils as templates, we have designed and characterized an all-D-amino-acid inhibitor of the fibril formation of the tau protein associated with Alzheimer's disease, and a non-natural L-amino-acid inhibitor of an amyloid fibril that enhances sexual transmission of human immunodeficiency virus. Our results indicate that peptides from structure-based designs can disrupt the fibril formation of full-length proteins, including those, such as tau protein, that lack fully ordered native structures. Because the inhibiting peptides have been designed on structures of dual-β-sheet 'steric zippers', the successful inhibition of amyloid fibril formation strengthens the hypothesis that amyloid spines contain steric zippers. 相似文献
123.
Dong-Hyung Cho Tomohiro Nakamura Stuart A. Lipton 《Cellular and molecular life sciences : CMLS》2010,67(20):3435-3447
Mitochondria are highly dynamic organelles that continuously undergo two opposite processes, fission and fusion. Mitochondrial
dynamics influence not only mitochondrial morphology, but also mitochondrial biogenesis, mitochondrial distribution within
the cell, cell bioenergetics, and cell injury or death. Drp1 mediates mitochondrial fission, whereas Mfn1/2 and Opa1 control
mitochondrial fusion. Neurons require large amounts of energy to carry out their highly specialized functions. Thus, mitochondrial
dysfunction is a prominent feature in a variety of neurodegenerative diseases. Mutations of Mfn2 and Opa1 lead to neuropathies
such as Charcot-Marie-Tooth disease type 2A and autosomal dominant optic atrophy. Moreover, both Aβ peptide and mutant huntingtin
protein induce mitochondrial fragmentation and neuronal cell death. In addition, mutants of Parkinson’s disease-related genes
also show abnormal mitochondrial morphology. This review highlights our current understanding of abnormal mitochondrial dynamics
relevant to neuronal synaptic loss and cell death in neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s
disease and Huntington’s disease. 相似文献
124.
The linear Gutenberg-Richter relationship is well-established. In any region of the Earth, the logarithm of the number of earthquakes, greater than any magnitude, is proportional to magnitude. This mea... 相似文献
125.
Crystal structure at 2.8 A resolution of a soluble form of the cell adhesion molecule CD2. 总被引:18,自引:0,他引:18
The crystal structure of a soluble form of the T lymphocyte antigen CD2 provides the first complete view of the extracellular region of a cell adhesion molecule. The topology of the molecule, which comprises two immunoglobulin-like domains, is the same as that of the first two domains of CD4 but the relative domain orientation is altered by a fairly flexible linker region. The putative ligand-binding beta-sheet forms a flat surface towards the top of the molecule. Crystal contacts between these surfaces suggest a plausible model for the adhesive interaction. 相似文献
126.
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128.
Chromosomes are divided into domains of open chromatin, where genes have the potential to be expressed, and domains of closed chromatin, where genes are not expressed. Classic examples of open chromatin domains include 'puffs' on polytene chromosomes in Drosophila and extended loops from lampbrush chromosomes. If multiple genes were typically expressed together from a single open chromatin domain, the position of co-expressed genes along the chromosomes would appear clustered. To investigate whether co-expressed genes are clustered, we examined the chromosomal positions of the genes expressed in the muscle of Caenorhabditis elegans at the first larval stage. Here we show that co-expressed genes in C. elegans are clustered in groups of 2-5 along the chromosomes, suggesting that expression from a chromatin domain can extend over several genes. These observations reveal a higher-order organization of the structure of the genome, in which the order of the genes along the chromosome id correlated with their expression in specific tissues. 相似文献
129.
Gardner MJ Hall N Fung E White O Berriman M Hyman RW Carlton JM Pain A Nelson KE Bowman S Paulsen IT James K Eisen JA Rutherford K Salzberg SL Craig A Kyes S Chan MS Nene V Shallom SJ Suh B Peterson J Angiuoli S Pertea M Allen J Selengut J Haft D Mather MW Vaidya AB Martin DM Fairlamb AH Fraunholz MJ Roos DS Ralph SA McFadden GI Cummings LM Subramanian GM Mungall C Venter JC Carucci DJ Hoffman SL Newbold C Davis RW Fraser CM Barrell B 《Nature》2002,419(6906):498-511
The parasite Plasmodium falciparum is responsible for hundreds of millions of cases of malaria, and kills more than one million African children annually. Here we report an analysis of the genome sequence of P. falciparum clone 3D7. The 23-megabase nuclear genome consists of 14 chromosomes, encodes about 5,300 genes, and is the most (A + T)-rich genome sequenced to date. Genes involved in antigenic variation are concentrated in the subtelomeric regions of the chromosomes. Compared to the genomes of free-living eukaryotic microbes, the genome of this intracellular parasite encodes fewer enzymes and transporters, but a large proportion of genes are devoted to immune evasion and host-parasite interactions. Many nuclear-encoded proteins are targeted to the apicoplast, an organelle involved in fatty-acid and isoprenoid metabolism. The genome sequence provides the foundation for future studies of this organism, and is being exploited in the search for new drugs and vaccines to fight malaria. 相似文献
130.
A mechanism for initiating RNA-dependent RNA polymerization 总被引:26,自引:0,他引:26