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991.
A salmonella protein antagonizes Rac-1 and Cdc42 to mediate host-cell recovery after bacterial invasion. 总被引:23,自引:0,他引:23
An essential feature of the bacterial pathogen Salmonella spp. is its ability to enter cells that are normally non-phagocytic, such as those of the intestinal epithelium. The bacterium achieves entry by delivering effector proteins into the host-cell cytosol by means of a specialized protein-secretion system (termed type III), which causes reorganization of the cell's actin cytoskeleton and ruffling of its membrane. One of the bacterial effectors that stimulates these cellular responses is SopE, which acts as a guanyl-nucleotide-exchange factor on Rho GTPase proteins such as Cdc42 and Rac. As the actin-cytoskeleton reorganization induced by Salmonella is reversible and short-lived, infected cells regain their normal architecture after bacterial internalization. We show here that the S. Typhimurium effector protein SptP, which is delivered to the host-cell cytosol by the type-III secretion system, is directly responsible for the reversal of the actin cytoskeletal changes induced by the bacterium. SptP exerts this function by acting as a GTPase-activating protein (GAP) for Rac-1 and Cdc42. 相似文献
992.
杨月红 《西安联合大学学报》1999,(2)
综述了近年来国内外在昆虫精子获能与顶体反应方面的研究概况,并系统地简述了昆虫精子顶体复合体基本结构,以及目前用于动物精子获能与顶体反应方面先进的方法和技术,同时对昆虫受精机理的研究进行了展望 相似文献
993.
X M Yin K Wang A Gross Y Zhao S Zinkel B Klocke K A Roth S J Korsmeyer 《Nature》1999,400(6747):886-891
The protein Bid is a participant in the pathway that leads to cell death (apoptosis), mediating the release of cytochrome c from mitochondria in response to signals from 'death' receptors known as TNFR1/Fas on the cell surface. It is a member of the proapoptotic Bcd-2 family and is activated as a result of its cleavage by caspase 8, one of a family of proteolytic cell-death proteins. To investigate the role of Bid in vivo, we have generated mice deficient for Bid. We find that when these mice are injected with an antibody directed against Fas, they nearly all survive, whereas wild-type mice die from hepatocellular apoptosis and haemorrhagic necrosis. About half of the Bid-deficient animals had no apparent liver injury and showed no evidence of activation of the effector caspases 3 and 7, although the initiator caspase 8 had been activated. Other Bid-deficient mice survived with only moderate damage: all three caspases (8 and 37) were activated but their cell nuclei were intact and no mitochondrial cytochrome c was released. We also investigated the effects of Bid deficiency in cultured cells treated with anti-Fas antibody (hepatocytes and thymocytes) or with TNFalpha. (fibroblasts). In these Bid-/- cells, mitochondrial dysfunction was delayed, cytochrome c was not released, effector caspase activity was reduced and the cleavage of apoptosis substrates was altered. This loss-of-function model indicates that Bid is a critical substrate in vivo for signalling by death-receptor agonists, which mediates a mitochondrial amplification loop that is essential for the apoptosis of selected cells. 相似文献
994.
J E Corrie B D Brandmeier R E Ferguson D R Trentham J Kendrick-Jones S C Hopkins U A van der Heide Y E Goldman C Sabido-David R E Dale S Criddle M Irving 《Nature》1999,400(6743):425-430
A new method is described for measuring motions of protein domains in their native environment on the physiological timescale. Pairs of cysteines are introduced into the domain at sites chosen from its static structure and are crosslinked by a bifunctional rhodamine. Domain orientation in a reconstituted macromolecular complex is determined by combining fluorescence polarization data from a small number of such labelled cysteine pairs. This approach bridges the gap between in vitro studies of protein structure and cellular studies of protein function and is used here to measure the tilt and twist of the myosin light-chain domain with respect to actin filaments in single muscle cells. The results reveal the structural basis for the lever-arm action of the light-chain domain of the myosin motor during force generation in muscle. 相似文献
995.
提出塑性损伤变量的定义,它由反映微空隙群的材料相对体积膨胀来表征.从理论上导出了塑性损伤变量Dp 与经典连续损伤力学中弹性损伤变量De= 1- E/E 之间的关系.根据此关系,用实验方法确定了聚合物材料HIPS在纵向拉伸过程中损伤变量的扩展 相似文献
996.
对聚合物材料HIPS进行了系统的变形-损伤试验研究.用提出的弹塑性损伤变量与关系分析了Ⅰ型裂纹端部的损伤场,给出了损伤场内非线性纵向应变分布与纵向应力分布.给出的损伤分析方法为进一步研究裂纹在损伤区内的稳定扩展奠定了新的基础 相似文献
997.
This paper studies on fabrics suitable for child patients'garment in the hospital environment in Hong Kong,China.Subjective measurement was carried out by questionnaire survey to consult medical staff on hospital requirement about fabric criteria for child patients' garment. On the other hand, objective measurement was conducted by performing laboratory tests on fabrics,which were sourced from commercial fabric market. Both measurements are evaluated according to the results on those fabric criteria in order to determine the most suitable kind of fabric for the end purpose. As a result of the comparison, it was found that T/C 1 scores the highest index. Therefore, it will be suggested for manufacturing child patients' garment to evaluate the fabric suitability to meet the wearers' requirement through hospital trial. 相似文献
998.
This paper described the physical behaviour of three types of denim cloths produced from rotor yarn, ring yarn and modified rotor yarn (prepared by adding conventional twist to rotor yarn) respectively. Experimental work showed that denim cloth produced from the modified rotor yarn has superior properties over conventional rotor yarn in terms of surface texture and appearance,tearing strength and resistance to abrasion. 相似文献
999.
一类矩阵方程的反对称正交反对称解及其最佳逼近 总被引:3,自引:0,他引:3
定义了一种新的矩阵类:反对称正交反对称矩阵,研究了一类矩阵方程的反对称正交反对称解的存在性及其最佳逼近问题。利用矩阵的广义奇异值分解,得到了该矩阵方程有反对称正交反对称解的充要条件及其通解表达式,并且给出了矩阵方程的解集合中与给定矩阵的最佳逼近。 相似文献
1000.
Aging appears to be an irreversible process. Here we report that nicotinamide (NAA) can induce rapid and reversible reversion
of aging phenotypes in human diploid fibroblasts in terms of cell morphology and senescence-associated β-galactosidase activity.
Although NAA seems to enhance the replicative potential of the cells, it has little effect on their growth rate and life span,
suggesting that NAA action is rather separated from the cellular replicative system. The effects are unique to NAA: none of
the NAA-related compounds examined (an NAD precursor/niacin, NAD analogs, and poly(ADP-ribose) polymerase inhibitors) exerted
similar effects. Thus, NAD-related metabolism and poly(ADP-ribosyl)ation are unlikely related to the NAA action. On the other
hand, histone acetyltransferase (HAT) activity was elevated in NAA-exposed cells, while in aged cells, HAT activity and histone
H4 acetylation were lowered. Taken together, the results suggest that NAA may cause rejuvenation by restoring, at least in
part, altered gene expression in aged cells through its activation of HAT.
Received 27 August 2001; received after revision 15 October 2001; accepted 15 October 2001 相似文献