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1.
Benzene, an accepted leukemogen, has been suggested to cause other hemato- and lymphopoietic cancers. Here we review the published literature for non-Hodgkin lymphoma (NHL) and occupational exposure to benzene. Six cohorts, sixteen case–control studies and two studies of other designs were identified through keyword searches of bibliographic databases. Twenty-two of twenty-four studies found no association between NHL and ever exposed to benzene compared to never; a random-effects meta-analysis gave a pooled risk estimate of 1.11 (95% confidence interval 0.94–1.30). Our finding of no effect agrees with one of two previous meta-analyses. The other meta-analysis examined if high benzene exposure increased NHL risk but a lack of consistent exposure categories within the same metric should have precluded pooling risks by exposure level. Instead, we reviewed whether dose–response relationships existed. The best available data came from six studies where exposure was estimated from historical measurements and on the whole, no trends in risks of NHL with rising cumulative, average, peak, or duration of benzene exposure were found. NHL is a heterogeneous group of malignancies and although less well-studied, benzene was not associated with any NHL subtype. In conclusion, benzene at either low or high doses does not increase the risk of NHL. 相似文献
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Eleanor LeBourdais 《CMAJ》1988,139(10):1002-1003
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To determine whether prolonged depolarization and/or changes in intracellular Ca2+ concentrations stimulate adaptive responses of neuronal nicotinic acetylcholine receptors, PC12 pheochromocytoma cells were grown in medium containing various concentrations of K+. Nicotinic receptor function was determined as carbachol-stimulated uptake of 86Rb+. Cells were exposed to 50 mM K+ for up to 4 days and then allowed to repolarize for 60 min. Under these conditions, no changes in basal or carbachol-stimulated uptake of 86Rb+ were observed. Furthermore, neither the time course of carbachol-stimulated uptake or the carbachol concentration dependence of 86Rb+ uptake was altered. Finally, concurrent depolarization did not affect the functional down-regulation produced by chronic exposure of the cells to carbachol. Thus, neuronal nicotinic acetylcholine receptors on PC12 cells do not appear to be regulated by depolarization or prolonged elevation of the intracellular Ca2+ level. 相似文献
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The metabolic profile of benzo[a]pyrene (BP) in cumene hydroperoxide-(CHP)-dependent reaction by male rat liver microsomes was dependent on CHP concentration. At 0.05 mM CHP, 3-hydroxy-BP was the major metabolite. Increase in CHP reduced 3-hydroxy-BP formation but increased BP quinone formation simultaneously. This change in metabolic profile was reversed by preincubation with pyrene. Pyrene (PY) selectively inhibited quinone formation but enhanced 3-hydroxy-BP formation. Naphthalene (NP) had no effect on BP quinone formation but inhibited BP 3-hydroxylation. Phenanthrene (PA) and benz[a]anthracene (BA) inhibited effectively 3-hydroxy-BP formation but only slightly quinone formation. BP binding to microsomal protein correlated to quinone formation and not BP 3-hydroxylation. BP metabolism by female rat liver microsomes also depended on CHP concentration but was much less efficient than the male. Quinones were consistently predominant metabolites and their formation was also inhibited by pyrene. Our data provide evidence that regioselectivity in BP metabolism involves at least two distinct binding sites. One site recognizes the benzo region of BP in BP 3-hydroxylation and the other recognizes the pyrene region in quinone formation. The different ratios of 3-hydroxy-BP to quinone formation by male and female rat liver microsomes suggest that the two binding sites are probably located at separate cytochrome P-450 isozymes. 相似文献
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Eleanor Leacock 《Dialectical Anthropology》1985,10(1-2):69-91
Conclusion Though relatively little direct attention has been given by Marxist anthropologists to a theory of individual behavior and thought in relation to societal processes, the above partial summary indicates the wealth of insight that is available for elaborating such a theory. In addition, there are of course significant developments in the field of psychology, notably the attention to activity as central to individual personality [], the renewed concern with levels of integration theory [], and the burgeoning interest in Vygotsky's writings on language, thought, and culture []. There are also the continuing attempts to locate Freud's positive contributions in a historical materialist frame [].Where, then, is psychological anthropology? As always, producing a richness of suggestive materials — such as those on varying conceptions of the self — but, as a glance at the pages of Ethos will show, unfortunately not engaged in fundamental theoretical innovation. By way of illustration, let me cite Spindler's The Making of Psychological Anthropology, a collection of articles by major figures, past and present. Spindler's introductory essay is thoughtful; always the teacher, he presents with consideration and modesty the history of the field, the disfavor into which it fell (in large part due to the methodlogical travesties of national character studies), and its stubborn persistence (following from the pervasive interest in the psychological dimension that has always characterized cultural anthropology). He summarizes ongoing problems as perceived from within the field, and as the major difficulty to be overcome pinpoints cultural overdeterminism and its inadequacy for explaining variations. The solution? Not the necessity of respecting history and focussing on how individuals variously understand and relate (according to their individual histories) to the established structures whereby particular societies produce, allocate, and consume basic goods, and how they variously respond to disjunctions in these structures even as they reproduce them. Instead Spindler writes, ... if we are to escape the double bind of our cultural overdeterminism, we are going to have to go beyond culture and even ecology, to biochemistry, to physiology and neurology, to genetics — to biology in the broadest sense of the term [].In closing, let me say to the reader, do not simply turn away in dismay. One must conclude that it is imperative to continue to build a solid alternative theory of relations among individual behaviors, individual understandings, cultural values, and societal processes, or, in other words, to replace a non-historical and essentially biological paradigm with a dialectical and materialist view of human action.Eleanor Leacock is Professor of Anthropology and Chair at the City College, City University of New York.
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Involvement of recA and exr Genes in the In Vivo Inhibition of the recBC Nuclease 总被引:13,自引:5,他引:8 下载免费PDF全文
Howard S. Marsden Ernest C. Pollard William Ginoza Eleanor P. Randall 《Journal of bacteriology》1974,118(2):465-470
When Escherichia coli cells are gamma irradiated they degrade their deoxyribonucleic acid (DNA). The DNA of previously gamma-irradiated T4 phage is also degraded in infected cells. The amount of degradation is not only dependent on the dose but also on the genotype of the cell. The amount of degradation is less in cells carrying a recB or a recC mutation, suggesting that most of the DNA degradation is due to the recB(+) and recC(+) gene product (exonuclease V). In some strains a previous dose of ultraviolet (UV) light followed by incubation renders the cells resistant to DNA degradation after gamma irradiation. We have shown this inhibition to take place for infecting T4 phage also. By using six strains of E. coli selected for mutations in the genes recA, exr (or lex), and uvrB, we have been able to show that the preliminary UV treatment produces no change in recA and exr cells for both endogenous DNA degradation and the degradation of infecting irradiated T4 phage DNA, i.e., inhibition was not detected in these strains. On the other hand, wild-type cells and strains carrying mutations of uvrB show inhibition in both types of experiments. Because the recA gene product and the exr(+) (lex(+)) gene product are necessary for the induction of prophage, it is possible that the phenomenon of inducible inhibition requires recA(+) and exr(+) presence. One interpretation of these results is that an inducible inhibitor may be controlled by the exr gene. 相似文献
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Most carcinogens, including polycyclic aromatic hydrocarbons (PAH), require metabolic activation to produce the ultimate electrophilic species that bind covalently with cellular macromolecules to trigger the cancer process. Metabolic activation of PAH can be understood in terms of two main pathways: one-electron oxidation to yield reactive intermediate radical cations and monooxygenation to produce bay-region diol epoxides. The reason we have postulated that one-electron oxidation plays an important role in the activation of PAH derives from certain common characteristics of the radical cation chemistry of the most potent carcinogenic PAH. Two main features common to these PAH are: 1) a relatively low ionization potential, which allows easy metabolic removal of one electron, and 2) charge localization in the PAH radical cation that renders this intermediate specifically and efficiently reactive toward nucleophiles. Equally important, cytochrome P-450 and mammalian peroxidases catalyze one-electron oxidation. This mechanism plays a role in the binding of PAH to DNA. Chemical, biochemical and biological evidence will be presented supporting the important role of one-electron oxidation in the activation of PAH leading to initiation of cancer. 相似文献