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961.
Kenneth L. Murphy Ingrid C. Burke Mary Ann Vinton William K. Lauenroth Martin R. Aguiar David A. Wedin Ross A. Virginia Petra N. Lowe 《植被学杂志》2002,13(3):395-402
Abstract. The central grassland region of North America is characterized by large gradients of temperature and precipitation. These climatic variables are important determinants of the distribution of plant species, and strongly influence plant morphology and tissue chemistry. We analysed regional patterns of plant litter quality as they vary with climate in grassland ecosystems throughout central North America including tall‐grass prairie, mixed grass prairie, shortgrass steppe, and hot desert grasslands. An extensive database from the International Biological Program and the Long‐Term Ecological Research Program allowed us to isolate the effects of climate from those of plant functional types on litter quality. Our analysis of grass species confirms a previously recognized positive correlation between C/N ratios and precipitation. Precipitation exhibited a similar positive relationship with lignin/N and percent lignin. Although there was no significant correlation between temperature and C/N, there was a significant positive relationship between temperature and both percent lignin and lignin/N. Among functional types, C3 grasses had a slightly lower C/N ratio than C4 grasses. Tall grass species exhibited higher C/N, lignin/N, and percent lignin than short grass species. This understanding of the regional patterns of litter quality and the factors controlling them provides us with a greater knowledge of the effect that global change and the accompanying feedbacks may have on ecosystem processes. 相似文献
962.
Yvonne E. G. Eskildsen-Helmond Han A. A. Van Heugten Jos M. J. Lamers 《Molecular and cellular biochemistry》1996,157(1-2):39-48
There is now clear evidence that receptor-dependent phospholipase D is present in myocardium. This novel signal transduction pathway provides an alternative source of 1,2-diacylglycerol, which activates isoforms of protein kinase C. The members of the protein kinase C family respond differently to various combinations of Ca2+, phosphatidylserine, molecular species of 1,2-diacylglycerol and other membrane phospholipid metabolites including free fatty acids. Protein kinase C isozymes are responsible for phosphorylation of specific cardiac substrate proteins that may be involved in regulation of cardiac contractility, hypertrophic growth, gene expression, ischemic preconditioning and electrophysiological changes. The initial product of phospholipase D, phosphatidic acid, may also have a second messenger role. As in other tissues, the question how the activity of phospholipase D is controlled by agonists in myocardium is controversial. Agonists, such as endothelin-1, atrial natriuretic factor and angiotensin 11 that are shown to activate phospholipase D, also potently stimulate phospholipase C- in myocardium. PMA stimulation of protein kinase C inactivates phospholipase C and strongly activates phospholipase D and this is probably a major mechanism by which agonists that promote phosphatidyl-4,5-bisphosphate hydrolysis secondary activate phosphatidylcholine-hydrolysis. On the other hand, one group has postulated that formation of phosphatidic acid secondary activates phosphatidyl-4,5-bisphosphate hydrolysis in cardiomyocytes. Whether GTP-binding proteins directly control phospholipase D is not clearly established in myocardium. Phospholipase D activation may also be mediated by an increase in cytosolic free Ca2+ or by tyrosine-phosphorylation. 相似文献
963.
Abstract: Arachidonic acid and oleoylacetylglycerol enhance depolarization-evoked glutamate release from hippocampal mossy fiber nerve endings. It was proposed this is a Ca2+ -dependent effect and that protein kinase C is involved. Here we report that arachidonic acid and oleoylacetylglycerol synergistically potentiate the glutamate release induced by the Ca2+ ionophore ionomycin. The Ca2+ dependence of this effect was established, as removal of Ca2+ eliminated evoked release and the lipid-dependent potentiation. Also, Ca2+ channel blockers attenuated ionomycin- and KCI-evoked exocytosis, as well as the facilitating effects of the lipid mediators. Although facilitation required Ca2+ , it may not involve an enhancement of evoked Ca2+ accumulation, because ionomycin-dependent glutamate release was potentiated under conditions that did not increase ionomycin-induced Ca2+ accumulation. Also, the facilitation may not depend on inhibition of K+ efflux, because enhanced release was observed in the presence of increasing concentrations of 4-aminopyridine and diazoxide did not reduce the lipid-dependent potentiation of exocytosis. In contrast, disruption of cytoskeleton organization with cytochalasin D occluded the lipid-dependent facilitations of both KCI- and ionomycin-evoked glutamate release. In addition, arachidonic acid plus glutamatergic or cholinergic agonists enhanced glutamate release, whereas a role for protein kinase C in the potentiation of exocytosis was substantiated using kinase inhibitors. It appears that the lipid-dependent facilitation of glutamate release from mossy fiber nerve endings requires Ca2+ and involves multiple presynaptic effects, some of which depend on protein kinase C. 相似文献
964.
M. J. Toth L. Huwyler W. C. Boyar A. F. Braunwalder D. Yarwood J. Hadala W. O. Haston M. A. Sills B. Seligmann N. Galakatos 《Protein science : a publication of the Protein Society》1994,3(8):1159-1168
We have determined which amino acids contribute to the pharmacophore of human C5a, a potent inflammatory mediator. A systematic mutational analysis of this 74-amino acid protein was performed and the effects on the potency of receptor binding and of C5a-induced intracellular calcium ion mobilization were measured. This analysis included the construction of hybrids between C5a and the homologous but unreactive C3a protein and site-directed mutagenesis. Ten noncontiguous amino acids from the structurally well-defined 4-helix core domain (amino acids 1-63) and the C-terminal arginine-containing tripeptide were found to contribute to the pharmacophore of human C5a. The 10 mostly charged amino acids from the core domain generally made small incremental contributions toward binding affinity, some of which were independent. Substitutions of the C-terminal amino acid Arg 74 produced the largest single effect. We also found the connection between these 2 important regions to be unconstrained. 相似文献
965.
丝裂素活化蛋白激酶参与内皮素刺激的兔主动脉平滑肌细胞增生 总被引:10,自引:1,他引:10
内皮素(endothelin,ET)是已知的体内活性最强的缩血管物质,其缩血管作用由G蛋白偶联受体所介导。但ET强大的促血管平滑肌细胞(VSMC)增生效应的机理尚未完全阐明。本研究选用培养的兔胸主动脉VSMC,探讨丝裂素活化蛋白激酶(MAPK)在ET促细胞增生中的作用。结果表明:ET-1呈时间和浓度依赖性地促进细胞摄取 ̄3H-TdR和激活MAPK,此作用可被蛋白激酶C(proteinkinaseC,PKC)抑制剂Staurosporine(STP),H-7和ET_A受体拮抗剂BQ123所抑制,但不被酪氨酸激酶抑制剂HerbimycinA(Herb)所抑制,用PKC激动剂PMA(Phorbolmyristateacetate)预处理VSMC,使其PKC活性下调,可显著减弱ET-1对MAPK的激活能力。本结果提示:(1)MAPK参与ET-1所致的VSMC增生;(2)ET-1促细胞增生与激活MAPK的作用是由ET_A受体和PKC介导的。 相似文献
966.
Protein Kinase C Activation Attenuates N-Methyl-d-Aspartate-Induced Increases in Intracellular Calcium in Cerebellar Granule Cells 总被引:1,自引:0,他引:1
Lawrence D. Snell Karen R. lorio Boris Tabakoff Paula L. Hoffman 《Journal of neurochemistry》1994,62(5):1783-1789
Abstract: Activation of the N-methyl-d -aspartate (NMDA) subtype of glutamate receptor increases levels of intracellular calcium and can lead to stimulation of protein kinase C activity. Several reports have demonstrated that stimulation of protein kinase C can, in turn, increase electrophysiological responses to NMDA in certain cells or in oocytes expressing certain NMDA receptor subunits. In the present study, the effects of protein kinase C activation on NMDA receptor-mediated increases in intracellular Ca2+ levels were investigated in primary cultures of rat cerebellar granule cells using fura-2 fluorescence spectroscopy. Pretreatment of the cells with the protein kinase C activator phorbol 12-myristate 13-acetate (PMA), but not the inactive analogue 4α-phorbol 12-myristate 13-acetate, inhibited NMDA-induced increases in intracellular Ca2+ levels. Coincubation of cells with PMA and the kinase inhibitor staurosporine or calphostin C blocked the PMA effect. The potency of NMDA was reduced twofold, and the potency of the NMDA receptor coagonist, glycine, to enhance the response to NMDA was decreased fourfold by pretreatment of cells with PMA. The effect on glycine was mimicked by pretreatment with okadaic acid, a protein phosphatase inhibitor. PMA treatment did not significantly alter Mg2+ inhibition of the NMDA response but decreased the potency of the competitive antagonist CGS-19755. These data suggest that, in cerebellar granule cells, the function of the NMDA receptor may be subject to feedback inhibition by protein kinase C stimulation. Under physiological conditions, this inhibition may result from a decreased effectiveness of the endogenous coagonists, glutamate and glycine. 相似文献
967.
摘要 目的:探讨急性肾损伤的危险因素及尿液可溶性程序性死亡受体1(spd-1)、白细胞介素18(IL-18)及胱抑素C(Cys-C)对急性肾损伤的预测价值。方法:选择2018年10月至2019年10月于我院就诊的急性肾损伤患者120例作为观察组,同时选取肾功能正常患者118例作为对照组,收集两组患者的临床资料,检测尿液spd-1、IL-18、Cys-C的含量,采用Logistic回归分析急性肾损伤的危险因素,并绘制ROC曲线,评估尿液spd-1、IL-18、Cys-C对急性肾损伤的预测价值。结果:观察组血清尿素氮(BUN)明显高于对照组(P<0.05)。观察组尿液spd-1、IL-18、Cys-C明显高于对照组(P<0.05)。Logistic回归分析结果显示,尿液spd-1(OR=1.461,P=0.000)、IL-18(OR=1.742,P=0.003)、Cys-C(OR=1.241,P=0.002)是急性肾损伤的危险因素。尿液spd-1预测急性肾损伤曲线下面积(AUC)为0.660,特异度为0.640,灵敏度为0.646;IL-18预测急性肾损伤的AUC为0.672,特异度为0.669,灵敏度为0.675;Cys-C预测急性肾损伤的AUC为0.643,特异度为0.649,灵敏度为0.673;三者联合检测预测急性肾损伤的AUC为0.792,特异度为0.667,灵敏度为0.917。结论:spd-1、IL-18、Cys-C在急性肾损伤患者尿液中含量明显增加,尿液spd-1、IL-18、Cys-C增加是急性肾损伤的危险因素,且三者联合检测对急性肾损伤的预测价值较高,具有一定的临床意义。 相似文献
968.
969.
Hirade K Tanabe K Niwa M Ishisaki A Nakajima K Nakamura M Sugiyama T Katagiri Y Kato K Kozawa O 《Journal of cellular biochemistry》2005,94(3):573-584
We previously reported that thrombin stimulates the induction of heat shock protein (HSP) 27 via p38 mitogen-activated protein (MAP) kinase activation in aortic smooth muscle A10 cells. In the present study, we investigated the effect of the adenylyl cyclase-cAMP system on the thrombin-stimulated induction of HSP27 in A10 cells. Forskolin, a direct activator of adenylyl cyclase, reduced the thrombin-induced p38 MAP kinase phosphorylation, and significantly suppressed the thrombin-stimulated accumulation of HSP27. However, dideoxyforskolin, a forskolin derivative that does not activate cAMP, failed to suppress the HSP27 accumulation. Furthermore, dibutyryl-cAMP (DBcAMP), a permeable analog of cAMP, significantly suppressed the accumulation of HSP27. On the other hand, calphostin C, an inhibitor of protein kinase C (PKC), reduced the thrombin-induced p38 MAP kinase phosphorylation, and significantly suppressed the thrombin-stimulated accumulation of HSP27. Moreover, forskolin reduced the p38 MAP kinase phosphorylation induced by the 12-O-tetradecanoylphorbol-13-acetate (TPA), a PKC-activating phorbol ester, and significantly suppressed the TPA-stimulated accumulation of HSP27. These results indicate that adenylyl cyclase-cAMP system has an inhibitory role in thrombin-stimulated HSP27 induction in aortic smooth muscle cells, and the effect seems to be exerted on the thrombin-induced PKC- p38 MAP kinase signaling pathway. 相似文献
970.
Regulated mRNA decay is essential for eukaryotic survival but the mechanisms for regulating global decay and coordinating it with growth, nutrient, and environmental cues are not known. Here we show that a signal transduction pathway containing the Pkh1/Pkh2 protein kinases and one of their effector kinases, Pkc1, is required for and regulates global mRNA decay at the deadenylation step in Saccharomyces cerevisiae. Additionally, many stresses disrupt protein synthesis and release mRNAs from polysomes for incorporation into P-bodies for degradation or storage. We find that the Pkh1/2-Pkc1 pathway is also required for stress-induced P-body assembly. Control of mRNA decay and P-body assembly by the Pkh-Pkc1 pathway only occurs in nutrient-poor medium, suggesting a novel role for these processes in evolution. Our identification of a signaling pathway for regulating global mRNA decay and P-body assembly provides a means to coordinate mRNA decay with other cellular processes essential for growth and long-term survival. Mammals may use similar regulatory mechanisms because components of the decay apparatus and signaling pathways are conserved. 相似文献