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241.
Mating strategies are sets of decisions aimed at maximizing reproductive success. For male animals, the fundamental problem that these strategies address is attaining mating access to females in a manner that maximizes their chances of achieving paternity. For chimpanzees (Pan troglodytes), despite substantial interest in mating strategies, very little attention has been paid to the most fundamental problem that mating strategies need to solve: finding mates. Only a single model, Dunbar's general model of male mating strategies, exists to explain mate‐searching behaviour in chimpanzees. Under this model, males in most populations are regarded as pursuing a ‘roving’ strategy: searching for and sequestering fertile females who are essentially passive with respect to mate searching. The roving mating strategy is an assumption deeply embedded in the way chimpanzee behaviour is considered; it is implicit in the conventional model for chimpanzee social structure, which posits that male ranging functions both to monitor female reproductive state and to ward these females from other groups of males through collective territoriality: essentially, ranging as mating effort. This perspective is, however, increasingly at odds with observations of chimpanzee behaviour. Herein, I review the logic and evidence for the roving‐male mating strategy and propose a novel alternative, a theoretical framework in which roving is a strategy pursued by female chimpanzees in order to engage successfully in promiscuous mating. Males, unable to thwart this female strategy, instead maximise the number of reproductive opportunities encountered by focusing their behaviour on countering threats to health, fertility and reproductive career. Their prolonged grooming bouts are seen, in consequence, as functioning to mitigate the negative impacts of socially induced physiological stress. In this new framework, the roving‐male strategy becomes, at best, a ‘best of a bad job’ alternative for low‐ranking males when faced with high levels of competition for mating access. Male chimpanzees do not search for mates, but for one another, for food, and, at times, for rivals in other communities. To the extent that female promiscuity functions to counter infanticide risk, mate searching by female chimpanzees—and any associated costs—can be seen as an unavoidable consequence of male sexual coercion. This novel framework is a better fit to the available data than is the conventional account. This review highlights the desperate need for additional work in an area of chimpanzee biology that has been somewhat neglected, perhaps in part because assumptions of roving males have remained unquestioned for too long. It also highlights the need, across taxa, to revisit and revise theory, and to test old assumptions, when faced with contrary data.  相似文献   
242.
Aim Ixodes scapularis is the most important vector of human tick‐borne pathogens in the United States, which include the agents of Lyme disease, human babesiosis and human anaplasmosis, among others. The density of host‐seeking I. scapularis nymphs is an important component of human risk for acquiring Borrelia burgdorferi, the aetiological agent of Lyme disease. In this study we used climate and field sampling data to generate a predictive map of the density of host‐seeking I. scapularis nymphs that can be used by the public, physicians and public health agencies to assist with the diagnosis and reporting of disease, and to better target disease prevention and control efforts. Location Eastern United States of America. Methods We sampled host‐seeking I. scapularis nymphs in 304 locations uniformly distributed east of the 100th meridian between 2004 and 2006. Between May and September, 1000 m2 were drag sampled three to six times per site. We developed a zero‐inflated negative binomial model to predict the density of host‐seeking I. scapularis nymphs based on altitude, interpolated weather station and remotely sensed data. Results Variables that had the strongest relationship with nymphal density were altitude, monthly mean vapour pressure deficit and spatial autocorrelation. Forest fragmentation and soil texture were not predictive. The best‐fit model identified two main foci – the north‐east and upper Midwest – and predicted the presence and absence of I. scapularis nymphs with 82% accuracy, with 89% sensitivity and 82% specificity. Areas of concordance and discordance with previous studies were discussed. Areas with high predicted but low observed densities of host‐seeking nymphs were identified as potential expansion fronts. Main conclusions This model is unique in its extensive and unbiased field sampling effort, allowing for an accurate delineation of the density of host‐seeking I. scapularis nymphs, an important component of human risk of infection for B. burgdorferi and other I. scapularis‐borne pathogens.  相似文献   
243.
The idea that competition and aggression are central to an understanding of the origins of group‐living and sociality among human and nonhuman primates is the dominant theory in primatology today. Using this paradigm, researchers have focused their attention on competitive and aggressive behaviors, and have tended to overlook the importance of cooperative and affiliative behaviors. However, cooperative and affiliative behaviors are considerably more common than agonistic behaviors in all primate species. The current paradigm often fails to explain the context, function, and social tactics underlying affiliative and agonistic behavior. Here, we present data on a basic question of primate sociality: how much time do diurnal, group‐living primates spend in social behavior, and how much of this time is affiliative and agonistic? These data are derived from a survey of 81 studies, including 28 genera and 60 species. We find that group‐living prosimians, New World monkeys, Old World monkeys, and apes usually devote less than 10% of their activity budget to active social interactions. Further, rates of agonistic behaviors are extremely low, normally less than 1% of the activity budget. If the cost to the actors of affiliative behavior is low even if the rewards are low or extremely variable, we should expect affiliation and cooperation to be frequent. This is especially true under conditions in which individuals benefit from the collective environment of living in stable social groups. Am J Phys Anthropol 128:84–97, 2005. © 2005 Wiley‐Liss, Inc.  相似文献   
244.
A central assumption of life history theory is that the evolution of the component traits is determined in part by trade-offs between these traits. Whereas the existence of such trade-offs has been well demonstrated, the relative importance of these remains unclear. In this paper we use optimality theory to test the hypothesis that the trade-off between present and future fecundity induced by the costs of continued growth is a sufficient explanation for the optimal age at first reproduction, alpha, and the optimal allocation to reproduction, G, in 38 populations of perch and Arctic char. This hypothesis is rejected for both traits and we conclude that this trade-off, by itself, is an insufficient explanation for the observed values of alpha and G. Similarly, a fitness function that assumes a mortality cost to reproduction but no growth cost cannot account for the observed values of alpha. In contrast, under the assumption that fitness is maximized, the observed life histories can be accounted for by the joint action of trade-offs between growth and reproductive allocation and between mortality and reproductive allocation (Individual Juvenile Mortality model). Although the ability of the growth/mortality model to fit the data does not prove that this is the mechanism driving the evolution of the optimal age at first reproduction and allocation to reproduction, the fit does demonstrate that the hypothesis is consistent with the data and hence cannot at this time be rejected. We also examine two simpler versions of this model, one in which adult mortality is a constant proportion of juvenile mortality [Proportional Juvenile Mortality (PJM) model] and one in which the proportionality is constant within but not necessarily between species [Specific Juvenile Mortality (SSJM) model]. We find that the PJM model is unacceptable but that the SSJM model produces fits suggesting that, within the two species studied, juvenile mortality is proportional to adult mortality but the value differs between the two species.  相似文献   
245.
Herein, a novel electrospun single‐ion conducting polymer electrolyte (SIPE) composed of nanoscale mixed poly(vinylidene fluoride‐co‐hexafluoropropylene) (PVDF‐HFP) and lithium poly(4,4′‐diaminodiphenylsulfone, bis(4‐carbonyl benzene sulfonyl)imide) (LiPSI) is reported, which simultaneously overcomes the drawbacks of the polyolefin‐based separator (low porosity and poor electrolyte wettability and thermal dimensional stability) and the LiPF6 salt (poor thermal stability and moisture sensitivity). The electrospun nanofiber membrane (es‐PVPSI) has high porosity and appropriate mechanical strength. The fully aromatic polyamide backbone enables high thermal dimensional stability of es‐PVPSI membrane even at 300 °C, while the high polarity and high porosity ensures fast electrolyte wetting. Impregnation of the membrane with the ethylene carbonate (EC)/dimethyl carbonate (DMC) (v:v = 1:1) solvent mixture yields a SIPE offering wide electrochemical stability, good ionic conductivity, and high lithium‐ion transference number. Based on the above‐mentioned merits, Li/LiFePO4 cells using such a SIPE exhibit excellent rate capacity and outstanding electrochemical stability for 1000 cycles at least, indicating that such an electrolyte can replace the conventional liquid electrolyte–polyolefin combination in lithium ion batteries (LIBs). In addition, the long‐term stripping–plating cycling test coupled with scanning electron microscope (SEM) images of lithium foil clearly confirms that the es‐PVPSI membrane is capable of suppressing lithium dendrite growth, which is fundamental for its use in high‐energy Li metal batteries.  相似文献   
246.
247.
Epidermal growth factor (EGF)–responsive stem cells from both developing and adult central nervous system (CNS) can be expanded and induced to differentiate into neurons and glia in vitro. Because of their self‐renewal and multipotent properties, these cells can potentially provide an unlimited tissue source for neural grafting in neurodegenerative disorders. However, the capability of neurons derived from these stem cells to project axons to distant targets following grafting, thereby enabling the restoration of damaged CNS circuitry, remains unknown. We hypothesize that grafted EGF‐responsive stem cells and their progeny are not competent to project axons into distant target sites unless exposed to specific neurotrophic factors. We compared neurite outgrowth between gestation day 14 primary mouse hippocampal cells and EGF‐generated secondary neurospheres of postnatal mouse hippocampal stem cells, following grafting onto the CA3 region of organotypic hippocampal slice cultures prepared from postnatal rats. Neurite outgrowth from grafted cells was visualized using immunohistochemical staining for the mouse specific antigen M6. Fetal hippocampal cells showed extensive and specific neurite outgrowth into many regions of the slice, including the CA1 region and distant subiculum, by 7 days after grafting. In contrast, neurite outgrowth from neurosphere cells was nonspecific and restricted to the immediate surrounding region after either 7 or even 15 days following grafting. Application of brain‐derived neurotrophic factor (BDNF) (5 ng in 0.5 μL) to slices on day 1 after grafting significantly enhanced neurite outgrowth from neurosphere cells, but overall neurite outgrowth from neurosphere cells remained decreased compared to that from fetal hippocampal cells. These results underscore that EGF‐responsive stem cell‐derived neurons possess limited intrinsic capability for long‐distance neurite outgrowth compared to fetal neurons. However, neurite outgrowth from EGF‐responsive stem cell–derived neurons can be enhanced by treating with specific neurotrophic factors such as BDNF. © 1999 John Wiley & Sons, Inc. J Neurobiol 38: 391–413, 1999  相似文献   
248.
The phenotypic traits of 7 independently isolated dam mutants of Escherichia coli have been examined. The mutant strains differ from the wildtype in the following respects: (1) decreased DNA adenine methylase activity in vivo and in vitro; (2) a 14--85-fold increase in spontaneous mutability; (3) decreased survival after ultraviolet irradiation; (4) a 10--21-fold increase in spontaneous induction of lambda phage from lysogens; (5) a 3--17-fold increase in the level of recombination; and (6) inviability of double mutants containing dam- and recB- or recC-. Unmethylated fd phage chromosomes are able to replicate normally in dam- mutants. A mutant strain in which the dcm gene is deleted is viable, showing that the dcm gene product is dispensible for growth.  相似文献   
249.
The yeast cytochrome bc1 complex, a component of the mitochondrial respiratory chain, is composed of ten distinct protein subunits. In the assembly of the bc1 complex, some ancillary proteins, such as the chaperone Bcs1p, are actively involved. The deletion of the nuclear gene encoding this chaperone caused the arrest of the bc1 assembly and the formation of a functionally inactive bc1 core structure of about 500-kDa. This immature bc1 core structure could represent, on the one hand, a true assembly intermediate or, on the other hand, a degradation product and/or an incorrect product of assembly. The experiments here reported show that the gradual expression of Bcs1p in the yeast strain lacking this protein was progressively able to rescue the bc1 core structure leading to the formation of the functional homodimeric bc1 complex. Following Bcs1p expression, the mature bc1 complex was also progressively converted into two supercomplexes with the cytochrome c oxidase complex. The capability of restoring the bc1 complex and the supercomplexes was also possessed by the mutated yeast R81C Bcsp1. Notably, in the human ortholog BCS1L, the corresponding point mutation (R45C) was instead the cause of a severe bc1 complex deficiency. Differently from the yeast R81C Bcs1p, two other mutated Bcs1p's (K192P and F401I) were unable to recover the bc1 core structure in yeast. This study identifies for the first time a productive assembly intermediate of the yeast bc1 complex and gives new insights into the molecular mechanisms involved in the last steps of bc1 assembly.  相似文献   
250.
STAT6 ASODN对哮喘小鼠脾淋巴细胞影响的实验研究   总被引:1,自引:0,他引:1  
目的研究STAT6反义寡核苷酸对哮喘小鼠脾淋巴细胞的影响作用。方法实验细胞分组:正常鼠空白组(A组)、正常鼠OVA组(B组)、哮喘空白组(C组)、哮喘OVA组(D组)、哮喘治疗组(E组)。正常设计并人工合成一段互补于小鼠STAT6 mRNA翻译起始区271-290的反义寡核苷酸片段,全链硫代修饰。用卵白蛋白和氢氧化铝复制哮喘模型,用淋巴细胞分离液分离脾淋巴细胞,进行体外培养并导入由阳离子脂质体转染剂Geneshuttle携带的反义寡核苷酸,观察反义寡核苷酸的转染对脾淋巴细胞STAT6蛋白表达水平及细胞培养上清中IL-4分泌水平的影响。免疫细胞化学观察脾淋巴细胞中STAT6蛋白的表达水平,同时采用酶联免疫吸附(ELISA)法测定脾细胞培养上清液中IL-4的浓度。结果D组细胞STAT6蛋白表达明显高于其余各组,均具有显著性差异(P均<0.01),STAT6 ASODN转染后,E组细胞该蛋白的表达量明显下降(P<0.01);D组脾淋巴细胞培养上清中IL-4分泌水平明显高于其余各组,均具有显著性差异(P均<0.01);STAT6 ASODN转染后,E组培养上清中IL-4分泌水平显著低于D组(P<0.01)。结论STAT6 ASODN可特异性抑制哮喘鼠脾淋巴细胞中STAT6蛋白的表达,并可特异性抑制脾淋巴细胞中IL-4的分泌,为反义基因技术治疗哮喘提供了依据。  相似文献   
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