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排序方式: 共有515条查询结果,搜索用时 15 毫秒
61.
62.
A map of the interactome network of the metazoan C. elegans 总被引:1,自引:0,他引:1
Li S Armstrong CM Bertin N Ge H Milstein S Boxem M Vidalain PO Han JD Chesneau A Hao T Goldberg DS Li N Martinez M Rual JF Lamesch P Xu L Tewari M Wong SL Zhang LV Berriz GF Jacotot L Vaglio P Reboul J Hirozane-Kishikawa T Li Q Gabel HW Elewa A Baumgartner B Rose DJ Yu H Bosak S Sequerra R Fraser A Mango SE Saxton WM Strome S Van Den Heuvel S Piano F Vandenhaute J Sardet C Gerstein M Doucette-Stamm L Gunsalus KC Harper JW Cusick ME Roth FP Hill DE Vidal M 《Science (New York, N.Y.)》2004,303(5657):540-543
63.
Yuwaraj K. Narnaware Bridget I. Baker Mike G. Tomlinson 《Fish physiology and biochemistry》1994,13(1):31-40
The effect of acute and chronic stress on the phagocytic activity of putative macrophages from the rainbow trout. Oncorhynchus mykiss has been assessed, using an in vitro phagocytic index, in which the average number of engulfed yeast cells in a population of phagocytes is determined. An injection
stress given under light anaesthesia, or a longer noise stress combined with confinement, both significantly reduced, within
3 h, the level of phagocytic activity of macrophages from the spleen and pronephros. Daily injection stress over six days
had a lesser effect on the proportion of phagocytically active cells even though plasma cortisol levels were equally raised.
Daily dexamethasone injection depressed the proportion of phagocytically active cells more than saline injection. In these
in vivo experiments, it was not possible to determine whether stress and steroids depressed the phagocytic activity of individual
macrophages or caused the active macrophages to migrate out of the spleen and pronephros. Administration of cortisol (200
nM) to trout macrophages in vitro failed to depress phagocytic activity within a 3h period but both α- and β-adrenergic agonists (10 μM) were usually depressive.
It is proposed that the autonomic nervous system may be an early regulator of macrophage phagocytosis following stress and
that corticosteroids only exert their suppressive effect on macrophage activity in the longer term.
To whom reprint requests should be addressed. 相似文献
64.
65.
Mike Greenblatt Christopher L. Brown Michael Lee Silvia Dauder Howard A. Bern 《Fish physiology and biochemistry》1989,6(5):261-278
Developmental profiles of thyroxin (T4), triiodothyronine (T3) and radioactive iodide uptake were established for eggs and T4 and T3 profiles were established for larvae (whole-body, yolk-only and body-only) of coho and chinook salmon. T4 and T3 were consistently present in all samples. In eggs, hormone levels remained fairly constant in all cohorst for at least the first three weeks of incubation, but then fluctuated in both directions in some sample groups. Large increases in T4 (from 9 ng/g to 245 ng/g) were seen in 1985 chinook eggs 28 days after fertilization. Radioactive iodide uptake (which was used as a possible indicator of thyroxinogenesis) increased at least 10-fold in both 1986 coho and chinook eggs from 23–30 days after fertilization. T4 (62 ng/g) and T3 (393 ng/g) were found in the bodies of 28-day-old 1986 chinook embryos. In whole larvae, hormone levels varied depending upon the cohort studied. In general, initial body-only concentrations of both T4 and T3 decreased as body weight increased, but before yolksac resorption was completed, both thyroid hormone content and concentration increased (except for chinook T3). T4 and T3 content in larval yolk stayed constant as yolksac size decreased, resulting in increased thyroid hormone concentration in the yolksac. All of these data suggest that the initial source of thyroid hormones in coho and chinook salmon eggs is maternal, but that by approximately 3–4 weeks after fertilization, the developing embryos begin to produce their own thyroid hormones. After hatching, increases in tissue T4 and T3 concentration coupled with constant T4 and T3 content in diminishing yolksacs suggest that larvae also produce their own thyroid hormones; yolksac content then may reflect both the original maternal hormones and the larva-producted hormones. 相似文献
66.
67.
Challenges of modeling ocean basin ecosystems 总被引:1,自引:0,他引:1
deYoung B Heath M Werner F Chai F Megrey B Monfray P 《Science (New York, N.Y.)》2004,304(5676):1463-1466
With increasing pressure for a more ecological approach to marine fisheries and environmental management, there is a growing need to understand and predict changes in marine ecosystems. Biogeochemical and physical oceanographic models are well developed, but extending these further up the food web to include zooplankton and fish is a major challenge. The difficulty arises because organisms at higher trophic levels are longer lived, with important variability in abundance and distribution at basin and decadal scales. Those organisms at higher trophic levels also have complex life histories compared to microbes, further complicating their coupling to lower trophic levels and the physical system. We discuss a strategy that builds on recent advances in modeling and observations and suggest a way forward that includes approaches to coupling across trophic levels and the inclusion of uncertainty. 相似文献
68.
Davis S Begon M De Bruyn L Ageyev VS Klassovskiy NL Pole SB Viljugrein H Stenseth NC Leirs H 《Science (New York, N.Y.)》2004,304(5671):736-738
In Kazakhstan and elsewhere in central Asia, the bacterium Yersinia pestis circulates in natural populations of gerbils, which are the source of human cases of bubonic plague. Our analysis of field data collected between 1955 and 1996 shows that plague invades, fades out, and reinvades in response to fluctuations in the abundance of its main reservoir host, the great gerbil (Rhombomys opimus). This is a rare empirical example of the two types of abundance thresholds for infectious disease-invasion and persistence- operating in a single wildlife population. We parameterized predictive models that should reduce the costs of plague surveillance in central Asia and thereby encourage its continuance. 相似文献
69.
Hillenmeyer ME Fung E Wildenhain J Pierce SE Hoon S Lee W Proctor M St Onge RP Tyers M Koller D Altman RB Davis RW Nislow C Giaever G 《Science (New York, N.Y.)》2008,320(5874):362-365
Genetics aims to understand the relation between genotype and phenotype. However, because complete deletion of most yeast genes ( approximately 80%) has no obvious phenotypic consequence in rich medium, it is difficult to study their functions. To uncover phenotypes for this nonessential fraction of the genome, we performed 1144 chemical genomic assays on the yeast whole-genome heterozygous and homozygous deletion collections and quantified the growth fitness of each deletion strain in the presence of chemical or environmental stress conditions. We found that 97% of gene deletions exhibited a measurable growth phenotype, suggesting that nearly all genes are essential for optimal growth in at least one condition. 相似文献
70.
MacArthur DG Balasubramanian S Frankish A Huang N Morris J Walter K Jostins L Habegger L Pickrell JK Montgomery SB Albers CA Zhang ZD Conrad DF Lunter G Zheng H Ayub Q DePristo MA Banks E Hu M Handsaker RE Rosenfeld JA Fromer M Jin M Mu XJ Khurana E Ye K Kay M Saunders GI Suner MM Hunt T Barnes IH Amid C Carvalho-Silva DR Bignell AH Snow C Yngvadottir B Bumpstead S Cooper DN Xue Y Romero IG; Genomes Project Consortium Wang J Li Y Gibbs RA McCarroll SA Dermitzakis ET Pritchard JK Barrett JC 《Science (New York, N.Y.)》2012,335(6070):823-828
Genome-sequencing studies indicate that all humans carry many genetic variants predicted to cause loss of function (LoF) of protein-coding genes, suggesting unexpected redundancy in the human genome. Here we apply stringent filters to 2951 putative LoF variants obtained from 185 human genomes to determine their true prevalence and properties. We estimate that human genomes typically contain ~100 genuine LoF variants with ~20 genes completely inactivated. We identify rare and likely deleterious LoF alleles, including 26 known and 21 predicted severe disease-causing variants, as well as common LoF variants in nonessential genes. We describe functional and evolutionary differences between LoF-tolerant and recessive disease genes and a method for using these differences to prioritize candidate genes found in clinical sequencing studies. 相似文献