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991.
Hypoxia induces a diverse spectrum of changes in the expression and activity of numerous DNA repair factors within the tumor microenvironment. In particular, we and others have shown that hypoxia induces phosphorylation and activation of the checkpoint kinase, CHK2, in an ATM-dependent manner. One downstream target of CHK2, the BRCA1 protein, plays a critical role in both DNA repair and cell cycle checkpoint regulation in mammalian cells. Here we report that BRCA1 is specifically phosphorylated on Serine 988 in response to hypoxic stress, and phosphorylation at this site is dependent on CHK2 expression. These findings enhance our understanding of ATM-CHK2 pathway activation in hypoxia, and they identify a novel role for BRCA1 in the response to hypoxic stress. 相似文献
992.
Guo B Sleper DA Sun J Nguyen HT Arelli PR Shannon JG 《TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik》2006,113(1):39-48
Quantitative trait locus (QTL) analysis on pooled data from multiple populations (pooled analysis) provides a means for evaluating, as a whole, evidence for existence of a QTL from different studies and examining differences in gene effect of a QTL among different populations. Objectives of this study were to: (1) develop a method for pooled analysis and (2) conduct pooled analysis on data from two soybean mapping populations. Least square interval mapping was extended for pooled analysis by inclusion of populations and cofactor markers as indicator variables and covariate variables separately in the multiple linear models. The general linear test approach was applied for detecting a QTL. Single population-based and pooled analyses were conducted on data from two F2:3 mapping populations, Hamilton (susceptible) × PI 90763 (resistant) and Magellan (susceptible) × PI 404198A (resistant), for resistance to soybean cyst nematode (SCN) in soybean. It was demonstrated that where a QTL was shared among populations, pooled analysis showed increased LOD values on the QTL candidate region over single population analyses. Where a QTL was not shared among populations, however, the pooled analysis showed decreased LOD values on the QTL candidate region over single population analyses. Pooled analysis on data from genetically similar populations may have higher power of QTL detection than single population-based analyses. QTLs were identified by pooled analysis on linkage groups (LGs) G, B1 and J for resistance to SCN race 2 whereas QTLs on LGs G, B1 and E for resistance to SCN race 5 in soybean PI 90763 and PI 404198A. QTLs on LG G and B1 were identified in both PI 90763 and PI 404198A whereas QTLs on LG E and J were identified in PI 90763 only. QTLs on LGs G and B1 for resistance to race 2 may be the same or closely linked with QTLs on LG G and B1 for resistance to race 5, respectively. It was further demonstrated that QTLs on G and B1 carried by PI 90763 were not significantly different in gene effect from QTLs on LGs G and B1 in PI 404198A, respectively. 相似文献
993.
994.
Raboin SJ Gulley S Henley SC Chan WC Esdaile AR Jackson CA Billups LH Sayegh AI 《Regulatory peptides》2006,134(2-3):141-148
Chemical sympathectomy with daily, intraperitoneal (IP) injections of guanethidine sulfate to adult rats, attenuated myenteric, but not dorsal vagal complex (DVC) Fos-like immunoreactivity (Fos-LI) by cholecystokinin-8 (CCK). This technique destroys only 60-70% of the sympathetic neurons, and spares the hormonal source of catecholamines, the adrenal medulla. The goal of the current study is to evaluate the effect of complete sympathectomy or destroying 100% of the sympathetic neurons by injecting guanethidine to 1-day-old pups (40 mg/kg daily for 5 weeks), and surgically removing the adrenal medulla. In the DVC, demedullation and sympathectomy-demedullation increased Fos-LI by CCK in the area postrema and nucleus of the solitary tract, but sympathectomy-demedullation increased it only in the area postrema. In the myenteric plexus, sympathectomy increased this response in the duodenum, and demedullation increased it in the duodenum and jejunum. On the other hand, sympathectomy-demedullation attenuated myenteric Fos-LI in the jejunum. These results indicate that catecholamines may play an inhibitory role on the activation of the DVC neurons by CCK. In the myenteric neurons, however, catecholamines may have both inhibitory and excitatory roles depending on the level of the intestine e.g., duodenum vs. jejunum. This may also indicate that CCK activates the enteric neurons by different mechanisms or through different pathways. 相似文献
995.
Grenier AL Abu-ihweij K Zhang G Ruppert SM Boohaker R Slepkov ER Pridemore K Ren JJ Fliegel L Khaled AR 《American journal of physiology. Cell physiology》2008,295(4):C883-C896
Apoptosis is a complex process essential for normal tissue development and cellular homeostasis. While biochemical events that occur late in the apoptotic process are better characterized, early physiological changes that initiate the progression of cell death remain poorly understood. Previously, we observed that lymphocytes, undergoing apoptosis in response to growth factor withdrawal, experienced a rapid and transient rise in cytosolic pH. We found that the protein responsible was the pH-regulating, plasma membrane protein Na+/H+ exchanger isoform 1 (NHE1), and that its activity was impeded by inhibition of the stress-activated kinase, p38 MAP kinase. In the current study, we examined how NHE1 is activated during apoptosis. We identified the phosphorylation sites on NHE1 that regulate its alkalinizing activity in response to a cell death stimulus. Performing targeted mutagenesis, we observed that substitution of Ser726 and Ser729 for alanines produced a mutant form of NHE1 that did not alkalinize in response to an apoptotic stimulus, and expression of which protected cells from serum withdrawal- induced death. In contrast, substitution of Ser726 and Ser729 for glutamic acids raised the basal pH and induced susceptibility to death. Analysis of serine phosphorylation showed that phosphorylation of NHE1 during apoptosis decreased upon mutation of Ser726 and Ser729. Our findings thus confirm a necessary function for NHE1 during apoptosis and reveal the critical regulatory sites that when phosphorylated mediate the alkalinizing activity of NHE1 in the early stages of a cell death response. pH; sodium hydrogen exchanger; mitogen-activated protein kinase 相似文献
996.
997.
998.
Shannon Atkinson Donald Calkins Vladimir Burkanov Michael Castellini Daniel Hennen Susan Inglis 《Marine Mammal Science》2008,24(2):276-289
A leading theory for the cause of the decline of Steller sea lions is nutritional stress, which led to chronic high juvenile mortality and possibly episodic adult mortality. Nutritional stress may have resulted from either poor quality or low abundance of prey. The objective of this study was to determine whether we could predict shifts in body condition (i.e., body mass or body fat content) over different seasons associated with a change in diet (i.e., toward lower quality prey). Captive Steller sea lions (n= 3) were fed three different diet regimes, where Diet 1 approximated the diet in the Kodiak area in the 1970s prior to the documented decline in that area, Diet 2 approximated the species composition in the Kodiak area after the decline had begun, and Diet 3 approximated the diet in southeast Alaska where the Steller sea lion population has been increasing for over 25 yr. All the animals used in this study were still growing and gained mass regardless of diet. Body fat (%) varied between 13% and 28%, but was not consistently high or low for any diet regime or season. Mean intake (in kg) of Diet 2 was significantly greater for all sea lions during all seasons. All animals did, however, tend to gain less body mass on Diets 2 and 3, as well as during the breeding and postbreeding seasons. They also tended to gain more mass during the winter and on Diet 1, though these differences were not statistically significant. Thus, changing seasonal physiology of Steller sea lions appears to have more impact on body condition than quality of prey, provided sufficient quantity of prey is available. Steller sea lions are opportunistic predators and are evidently able to thrive on a variety of prey. Our results indicate that Steller sea lions are capable of compensating for prey of low quality. 相似文献
999.
Julia Schuckel Shannon Meisner Päivi H. Torkkeli Andrew S. French 《Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology》2008,194(5):483-489
Time-dependent properties of chemical signals are probably crucially important to many animals, but little is known about
the dynamics of chemoreceptors. Behavioral evidence of dynamic sensitivity includes the control of moth flight by pheromone
plume structure, and the ability of some blood-sucking insects to detect varying concentrations of carbon dioxide, possibly
matched to host breathing rates. Measurement of chemoreceptor dynamics has been limited by the technical challenge of producing
controlled, accurate modulation of olfactory and gustatory chemical concentrations over suitably wide ranges of amplitude
and frequency. We used a new servo-controlled laminar flow system, combined with photoionization detection of surrogate tracer
gas, to characterize electroantennograms (EAG) of Drosophila antennae during stimulation with fruit odorants or aggregation pheromone in air. Frequency response functions and coherence
functions measured over a bandwidth of 0–100 Hz were well characterized by first-order low-pass linear filter functions. Filter
time constant varied over almost a tenfold range, and was characteristic for each odorant, indicating that several dynamically
different chemotransduction mechanisms are present. Pheromone response was delayed relative to fruit odors. Amplitude of response,
and consequently signal-to-noise ratio, also varied consistently with different compounds. Accurate dynamic characterization
promises to provide important new information about chemotransduction and odorant-stimulated behavior. 相似文献
1000.
Shannon S Allen Whitney Evans James Carlisle Rana Hajizadeh Michele Nadaf Bryan E Shepherd David T Pride Joyce E Johnson Wonder P Drake 《Respiratory research》2008,9(1):36