全文获取类型
收费全文 | 5313篇 |
免费 | 514篇 |
专业分类
5827篇 |
出版年
2022年 | 32篇 |
2021年 | 76篇 |
2020年 | 40篇 |
2019年 | 55篇 |
2018年 | 61篇 |
2017年 | 57篇 |
2016年 | 89篇 |
2015年 | 186篇 |
2014年 | 206篇 |
2013年 | 275篇 |
2012年 | 324篇 |
2011年 | 323篇 |
2010年 | 221篇 |
2009年 | 208篇 |
2008年 | 274篇 |
2007年 | 271篇 |
2006年 | 268篇 |
2005年 | 259篇 |
2004年 | 239篇 |
2003年 | 215篇 |
2002年 | 202篇 |
2001年 | 64篇 |
2000年 | 54篇 |
1999年 | 65篇 |
1998年 | 60篇 |
1997年 | 53篇 |
1996年 | 39篇 |
1995年 | 45篇 |
1994年 | 47篇 |
1993年 | 49篇 |
1992年 | 55篇 |
1991年 | 35篇 |
1990年 | 61篇 |
1989年 | 57篇 |
1988年 | 46篇 |
1987年 | 54篇 |
1986年 | 37篇 |
1984年 | 68篇 |
1983年 | 55篇 |
1982年 | 60篇 |
1981年 | 44篇 |
1980年 | 41篇 |
1979年 | 32篇 |
1978年 | 37篇 |
1976年 | 34篇 |
1974年 | 41篇 |
1973年 | 32篇 |
1971年 | 37篇 |
1970年 | 33篇 |
1965年 | 32篇 |
排序方式: 共有5827条查询结果,搜索用时 0 毫秒
51.
J. P. Monson R. M. Henderson J. A. Smith R. A. Iles M. Faus-Dader N. D. Carter R. Heath H. Metcalfe R. D. Cohen 《Bioscience reports》1984,4(10):819-825
In perfused rat liver a decrease of cytosol pH, determined with pH-sensitive microelectrodes7 from 7.2 to 6.85 is associated with a 50% fall in ureogenesis from ammonium chloride. In isolated rat hepatocytes the fall in ureogenesis due to acidosis is associated with decrease in the mitochondrial and cytosolic concentration of citrulline. Limitation of carbamoyl phosphate synthesis and thus citrulline supply could be responsible for the inhibition of ureogenesis observed. 相似文献
52.
J.M. Gennity Nestor R. Bottino Ralph A. Zingaro Andrew E. Wheeler Kurt J. Irgolic 《Biochemical and biophysical research communications》1984,118(1):176-182
Axenic cultures of the green algae and red algae were grown in the presence of sublethal quantities of selenite. All purified lipids from both algae were found to contain bound selenium, except for saturated hydrocarbons. Of the lipids which contain selenium, carotenoid pigments contain the greatest concentrations. Lipid-associated selenium is not metabolically incorporated. The selenium is probably non-covalently bound to the lipids. 相似文献
53.
Plants and fungi possess an outwardly directed plasma membrane proton pump that may regulate intracellular pH. We provide the first demonstration that amoebae of the slime mould Dictyostelium discoideum also possess a similar proton pump. It can be assayed either as an ATPase activity in highly purified plasma membranes or as a proton pump, after solubilization and reconstruction into liposomes. The pump is inhibited by vanadate, diethylstilbestrol (DES) and miconazole but not by azide or ouabain. The proton pump described here may represent the target for the action of DES and miconazole, both of which have previously been shown to induce stalk cell formation during the in vitro development of Dictyostelium. 相似文献
54.
55.
56.
We show that DNA gyrase is required for transposition of Tn5. Coumermycin, a potent inhibitor of DNA gyrase subunit B, inhibits transposition in a wild-type strain, but has no effect on strains carry ing a coumermycin-resistant allele in gyrB. In addition, strains containing a thermolabile subunit A of gyrase (gyrA43) are defective for transposition at a nonpermissive temperature. The requirement for gyrase is due to a requirement for supercoiled DNA. We showed this by introducing into the gyrA43 strain a deletion of the gene encoding topoisomerase I. The introduction of the second mutation caused an increase in the superhelical density of DNA as well as an increase in the transposition frequency. This also implies that if the DNA is supercoiled there is no further requirement for gyrase. Experiments with coumermycin support this, because the drug does not inhibit transposition if the recipient DNA remains supercoiled. This indicates that if the DNA acting as recipient of the transposon is deficient in supercoils, it will be a poor substrate for transposition. We also describe a system in which a gene on a multicopy plasmid can be efficiently introduced into the Escherichia coli chromosome. 相似文献
57.
Methylation mediated by S-adenosyl-l-methionine is required for the chemotaxis of mononuclear leukocytes. We investigated whether transmethylation reactions are required for normal functioning of chemotactic factor receptors. Three chemoattracrant-mediated functions in macrophages, chemotaxis, the stimulated release of arachidonic acid from membrane phospholipids and superoxide production, are markedly depressed by agents that inhibit cellular methylation reactions. Treatment of macrophages with methylation inhibitors decreased the affinity of the N-formylated chemoattractant receptor present on these cells by a factor of 4.5, but did not significantly alter the total receptor number. These results suggest that the N-formylated chemoattractant receptor on macrophages can exist in more than one affinity state and that an ongoing methylation reaction is required for the maintenance of the receptor in its higher affinity form. Inhibition of methylation lowers the affinity of the receptor and renders it no nfunctional or “uncoupled” in its ability to produce chemotaxis, superoxide and the release of arachidonic acid from leukocyte membranes. 相似文献
58.
59.
M K Hoffmann S Koenig R S Mittler H F Oettgen P Ralph C Galanos U Hammerling 《Journal of immunology (Baltimore, Md. : 1950)》1979,122(2):497-502
Peritoneal macrophages of the mouse produce, in response to cell wall components of Gram-negative bacteria (lipopolysaccharide and lipoproteins), a factor that causes antigen-stimulated B cells of differentiate into antibody-producing cells. Unlike lipopolysaccharide, this factor is not mitogenic for B cells. Production of the macrophage factor does not depend on participation of T cells or other accessory cells since it is readily produced by several cloned macrophage cell lines as well as by peritoneal macrophages of athymic nude mice. The factor is active only in conjunction with antigen. T cells, although apparently not necessary, amplify its effect. The factor induces phenotypic differentiation of B cell precursors as selectively as thymopoietin induces differentiation of prothymocytes. 相似文献
60.
Anke M. Mans Julien F. Biebuyck Stuart J. Saunders Ralph E. Kirsch Richard A. Hawkins 《Journal of neurochemistry》1979,33(2):409-418
Abstract— Tryptophan transport across the blood-brain barrier was studied using a single injection dual isotope label technique, in the following three conditions: normal rats, rats with portacaval shunts, and rats with portacaval shunts followed 65 h later by hepatic artery ligation. In both normal rats and those with acute hepatic failure the tryptophan transport system was found to be comprised of two kinetically distinct components. One component was saturable and obeyed Michaelis-Menten kinetics (normal: Vmax= 19.5 nmol.min?1.g?1. Km= 113 μM; hepatic failure: Vmax, = 33.8 nmol.min?1.g?1, Km= 108 μM), and the second was a high capacity system which transported tryptophan in direct proportion to concentration over the range tested (normal: K= 0.026 ml.min?1.g?1; hepatic failure: K= 0.067 ml.min?1.g?1). Since the saturable low capacity component transports several neutral amino acids, and their collective plasma concentration is high in relation to the individual Kms, tryptophan transport by this component is reduced by competitive inhibition under physiological conditions. Thus it was calculated that in normal rats approx 40% of tryptophan influx occurs via the high capacity system. During acute hepatic failure transport via both components was increased substantially, approximately doubling the rate of tryptophan penetration of the blood-brain barrier at all concentrations tested. The contribution by the high capacity component became even more significant than in normal rats, accounting for about 75% of all tryptophan passage from plasma to brain. Brain tryptophan content was 29.9 nmol/g in normal rats and rose to 45.2 nmol/g in rats with portacaval shunts and 50.5 nmol/g in those with acute hepatic failure, correlating with the increased rate of tryptophan transport. In a previous study we found that plasma competing amino acids were greatly increased during acute hepatic failure. Calculations predict that these increased concentrations would cause a reduction in tryptophan transport by the low capacity system. However, because of the increase in the rate of transport by the high capacity component, net tryptophan entry across the blood-brain barrier was actually increased. This increased rate of transport clearly contributes to the increased content of brain tryptophan found during hepatic failure. 相似文献