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141.
J. L. Scaro C. Miranda M. A. Carrera B. Martin I. Torrejon 《Cellular and molecular life sciences : CMLS》1984,40(4):348-350
Summary Removal of 15% of blood volume in the mouse increases erythropoiesis by a factor of 2.2 when measured 12 h after bleeding. Exposure of normal mice to 40% reduced barometric pressure for the same period of time increases erythropoiesis only by a factor of 1.6. The response to hypoxia takes place in the presence of a 40% reduction of oxygen consumption and tissue-venous Po
2, changes which are concomitant with a 5-fold increase in plasma erythropoietin activity. The larger response in anemic animals on the other hand occurs without any detectable change in these parameters. These results cast serious doubts about the interpretation of the quantitative homeostatic control of erythropoiesis based solely on the action of erythropoietin.Acknowledgments. This work was supported by a grant from the Consejo Nacional de Investigaciones Científicas y Técnicas de la República Argentina. We thank Isabel Zingariello for excellent technical assistance. 相似文献
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Nandkumar S. Shah L. E. Fox S. P. Martin 《Cellular and molecular life sciences : CMLS》1966,22(10):648-649
Zusammenfassung Bei den tuberkulösen Meerschweinchen wurde in der Niere eine erhöhte Aktivität der Glukose-6-Phosphatase beobachtet. Isoniazid hat die erhöhte Aktivität des Enzyms nicht erniedrigt, wenn es tuberkulösen Tieren vom 8. bis zum 38. Tage nach der Infektion oral verabreicht wurde. Es wird angenommen, dass die erhöhte Aktivität Ausdruck der Adaptionsfähigkeit von Glukose-6-Phosphatase ist.
Galesburg State Research Hospital, Galesburg, Illinois, USA. 相似文献
Galesburg State Research Hospital, Galesburg, Illinois, USA. 相似文献
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147.
Martin Niss 《Archive for History of Exact Sciences》2005,59(3):267-318
I chart the considerable changes in the status and conception of the Lenz-Ising model from 1920 to 1950 in terms of three phases: In the early 1920s, Lenz and Ising introduced the model in the field of ferromagnetism. Based on an exact derivation, Ising concluded that it is incapable of displaying ferromagnetic behavior, a result he erroneously extended to three dimensions. In the next phase, Lenz and Isings contemporaries rejected the model as a representation of ferromagnetic materials because of its conflict with the new quantum mechanics. In the third phase, from the early 1930s to the early 1940s, the model was revived as a model of cooperative phenomena. I provide more detail on this history than the earlier accounts of Brush (1967) and Hoddeson, Schubert, Heims, and Baym (1992) and question some of their conclusions. Moreover, my account differs from these in its focus on the development of the model in its capacity as a model. It examines three aspects of this development: (1) the attitudes on the degree of physical realism of the Lenz-Ising model in its representation of physical phenomena; (2) the various reasons for studying and using it; and (3) the effect of the change in its theoretical basis during the transition from the old to the new quantum mechanics. A major theme of my study is that even though the Lenz-Ising model is not fully realistic, it is more useful than more realistic models because of its mathematical tractability. I argue that this point of view, important for the modern conception of the model, is novel and that its emergence, while perhaps not a consequence of its study, is coincident with the third phase of its development. 相似文献
148.
TRPC6 is a glomerular slit diaphragm-associated channel required for normal renal function 总被引:27,自引:0,他引:27
Reiser J Polu KR Möller CC Kenlan P Altintas MM Wei C Faul C Herbert S Villegas I Avila-Casado C McGee M Sugimoto H Brown D Kalluri R Mundel P Smith PL Clapham DE Pollak MR 《Nature genetics》2005,37(7):739-744
Progressive kidney failure is a genetically and clinically heterogeneous group of disorders. Podocyte foot processes and the interposed glomerular slit diaphragm are essential components of the permeability barrier in the kidney. Mutations in genes encoding structural proteins of the podocyte lead to the development of proteinuria, resulting in progressive kidney failure and focal segmental glomerulosclerosis. Here, we show that the canonical transient receptor potential 6 (TRPC6) ion channel is expressed in podocytes and is a component of the glomerular slit diaphragm. We identified five families with autosomal dominant focal segmental glomerulosclerosis in which disease segregated with mutations in the gene TRPC6 on chromosome 11q. Two of the TRPC6 mutants had increased current amplitudes. These data show that TRPC6 channel activity at the slit diaphragm is essential for proper regulation of podocyte structure and function. 相似文献
149.
Jadeja S Smyth I Pitera JE Taylor MS van Haelst M Bentley E McGregor L Hopkins J Chalepakis G Philip N Perez Aytes A Watt FM Darling SM Jackson I Woolf AS Scambler PJ 《Nature genetics》2005,37(5):520-525
Fraser syndrome is a recessive, multisystem disorder presenting with cryptophthalmos, syndactyly and renal defects and associated with loss-of-function mutations of the extracellular matrix protein FRAS1. Fras1 mutant mice have a blebbed phenotype characterized by intrauterine epithelial fragility generating serous and, later, hemorrhagic blisters. The myelencephalic blebs (my) strain has a similar phenotype. We mapped my to Frem2, a gene related to Fras1 and Frem1, and showed that a Frem2 gene-trap mutation was allelic to my. Expression of Frem2 in adult kidneys correlated with cyst formation in my homozygotes, indicating that the gene is required for maintaining the differentiated state of renal epithelia. Two individuals with Fraser syndrome were homozygous with respect to the same missense mutation of FREM2, confirming genetic heterogeneity. This is the only missense mutation reported in any blebbing mutant or individual with Fraser syndrome, suggesting that calcium binding in the CALXbeta-cadherin motif is important for normal functioning of FREM2. 相似文献
150.
Sickle cell anemia (SCA) is a paradigmatic single gene disorder caused by homozygosity with respect to a unique mutation at the beta-globin locus. SCA is phenotypically complex, with different clinical courses ranging from early childhood mortality to a virtually unrecognized condition. Overt stroke is a severe complication affecting 6-8% of individuals with SCA. Modifier genes might interact to determine the susceptibility to stroke, but such genes have not yet been identified. Using Bayesian networks, we analyzed 108 SNPs in 39 candidate genes in 1,398 individuals with SCA. We found that 31 SNPs in 12 genes interact with fetal hemoglobin to modulate the risk of stroke. This network of interactions includes three genes in the TGF-beta pathway and SELP, which is associated with stroke in the general population. We validated this model in a different population by predicting the occurrence of stroke in 114 individuals with 98.2% accuracy. 相似文献