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71.
72.
Markus Kurz Karin Schütz Michael Göbel 《Origins of life and evolution of the biosphere》1996,26(3-5):263-264
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Heidrun Herrmann Christian Müller Ingmar Schmidt Jens Mahnke Lothar Petruschka Karin Hahnke 《Molecular genetics and genomics : MGG》1995,247(2):240-246
The genetic organization of the DNA region encoding the phenol degradation pathway ofPseudomonas putida H has been investigated. This strain can utilize phenol or some of its methylated derivatives as its sole source of carbon and energy. The first step in this process is the conversion of phenol into catechol. Catechol is then further metabolized via themeta-cleavage pathway into TCA cycle intermediates. Genes encoding these enzymes are clustered on the plasmid pPGH1. A region of contiguous DNA spanning about 16 kb contains all of the genetic information necessary for inducible phenol degradation. The analysis of mutants generated by insertion of transposons and cassettes indicates that all of the catabolic genes are contained in a single operon. This codes for a multicomponent phenol hydroxylase andmeta-cleavage pathway enzymes. Catabolic genes are subject to positive control by the gene product(s) of a second locus. 相似文献
75.
Effects of Nerve Growth Factor on Glutathione Peroxidase and Catalase in PC 12 Cells 总被引:4,自引:1,他引:3
Deepa Sampath George R. Jackson Karin Werrbach-Perez J. Regino Perez-Polo 《Journal of neurochemistry》1994,62(6):2476-2479
Abstract: Nerve growth factor (NGF) is a member of the neuro- trophin family and is required for the survival and maintenance of peripheral sympathetic and sensory ganglia. In the CNS, NGF regulates cholinergic expression by basal forebrain cholinergic neurons. NGF also stimulates cellular resistance to oxidative stress in the PC12 cell line and protects PC12 cells from the toxic effects of reactive oxygen species. The hypothesis that NGF protection involves changes in antioxidant enzyme expression was tested by measuring its effects on catalase and glutathione per- oxidase (GSH Px) mRNA expression in PC12 cells. NGF increased catalase and GSH Px mRNA levels in PC 12 cells in a time- and dose-dependent manner. There was also a corresponding increase in the enzyme activities of catalase and GSH Px. Thus, NGF can provide cytoprotection to PC12 cells by inducing the free radical scavenging enzymes catalase and GSH Px. 相似文献
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Classes and mechanisms of calcium waves 总被引:3,自引:0,他引:3
The best known calcium waves move at about 5–30 μm/s (at 20°C) and will be called fast waves to distinguish them from slow (contractile) ones which move at 0.1-1 μm/s as well as electrically propagated, ultrafast ones. Fast waves move deep within cells and seem to underlie most calcium signals. Their velocity and hence mechanism has been remarkably conserved among all or almost all eukaryotic cells. In fully active (but not overstimulated) cells of all sorts, their mean speeds lie between about 15–30 μm/s at 20°C. Their amplitudes usually lie between 3–30 μM and their frequencies from one per 10–300 s. They are propagated by a reaction diffusion mechanism governed by the Luther equation in which Ca2+ ions are the only diffusing propagators, and calcium induced calcium release, or CICR, the only reaction; although this reaction traverses various channels which are generally modulated by IP3 or cADPR. However, they may be generally initiated by a second, lumenal mode of CICR which occurs within the ER. Moreover, they are propagated between cells by a variety of mechanisms. Slow intracellular waves, on the other hand, may be mechanically propagated via stretch sensitive calcium channels. 相似文献
79.
The induction of long-term potentiation (LTP) is generally assumed to be triggered by Ca2+ entry into dendritic spines via NMDA receptor-gated channels. A previous computational model proposed that spines serve several functions in this process. First, they compartmentalize and amplify increases in [Ca2+]i. Second, they augment the nonlinear relationship between synaptic strength and the probability or magnitude of LTP induction. Third, they isolate the metabolic machinery responsible for LTP induction from increases in [Ca2+]i produced by voltage-gated Ca2+ channels in the dendritic shaft. Here we examine this last prediction of the model using methods that combine confocal microscopy with simultaneous neurophysiological recordings in hippocampal brain slices. Either of two Ca2+-sensitive dyes were injected into CA1 pyramidal neurons. Direct depolarization of the neurons via the somatic electrode produced clear increases in Ca2+ signals within the dendritic spines, a result that was not predicted by the previous spine model. Our new spine model suggests that some of this signal could theoretically result from Ca2+-bound dye diffusing from the dendritic shaft into the spine. Dye diffusion alone cannot, however, explain the numerous cases in which the Ca2+ signal in the spine was considerably larger than that in the adjacent dendritic shaft. The latter observations raise the possiblity of voltage-gated Ca2+ entry directly into the spine or else perhaps via Ca2+-dependent Ca2+release. The new spine model accommodates these observations as well as several other recent experimental results. 1994 John Wiley & Sons, Inc. 相似文献
80.
Regulation of γ-Aminobutyric Acid Synthesis in the Brain 总被引:3,自引:3,他引:0
Abstract: γ-Aminobutyric acid (GABA) is synthesized in brain in at least two compartments, commonly called the transmitter and metabolic compartments, and because reglatory processes must serve the physiologic function of each compartment, the regulation of GABA synthesis presents a complex problem. Brain contains at least two molecular forms of glutamate decarboxylase (GAD), the principal synthetic enzyme for GABA. Two forms, termed GAD65 and GAD67, are the products of two genes and differ in sequence, molecular weight, interaction with the cofactor, pyridoxal 5′-phosphate (pyridoxal-P), and level of expression among brain regions. GAD65 appears to be localized in nerve terminals to a greater degree than GAD67, which appears to be more uniformly distributed throughout the cell. The interaction of GAD with pyridoxal-P is a major factor in the short-term regulation of GAD activity. At least 50% of GAD is present in brain as apoenzyme (GAD without bound cofactor; apoGAD), which serves as a reservoir of inactive GAD that can be drawn on when additional GABA synthesis is needed. A substantial majority of apoGAD in brain is accounted for by GAD65, but GAD67 also contributes to the pool of apoGAD. The apparent localization of GAD65 in nerve terminals and the large reserve of apo-GAD65 suggest that GAD65 is specialized to respond to short-term changes in demand for transmitter GABA. The levels of apoGAD and the holoenzyme of GAD (holoGAD) are controlled by a cycle of reactions that is regulated by physiologically relevant concentrations of ATP and other polyanions and by inorganic phosphate, and it appears possible that GAD activity is linked to neuronal activity through energy metabolism. GAD is not saturated by glutamate in synaptosomes or cortical slices, but there is no evidence that GABA synthesis in vivo is regulated physiologically by the availability of glutamate. GABA competitively inhibits GAD and converts holo- to apoGAD, but it is not clear if intracellular GABA levels are high enough to regulate GAD. There is no evidence of short-term regulation by second messengers. The syntheses of GAD65 and GAD67 proteins are regulated separately. GAD67 regulation is complex; it not only is present as apoGAD67, but the expression of GAD67 protein is regulated by two mechanisms: (a) by control of mRNA levels and (b) at the level of translation or protein stability. The latter mechanism appears to be mediated by intracellular GABA levels. 相似文献