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21.
Evolutionary stability (sensu Maynard Smith: Evolution and the Theory of Games, Cambridge: Cambridge University Press, 1982) of TIT FOR TAT (TFT) under the social ecology of the iterated Prisoner's Dilemma is a function of the number of pure TFT groups (dyads) in the population, relative to the social position of a focal invading defector. Defecting against TFT always raises the defector's relative intragroup fitness; when Axelrod's (Am. Polit. Sci. Rev. 75:306–318, 1981; The Evolution of Cooperation. New York: Basic Books, 1984) Evolutionary stable strategy (ESS) conditions are met, defection also lowers the absolute fitness of the defector. Here the retaliatory (punishing) character of TFT converts defection into spite, permitting pure TFT groups to sufficiently outproduce the defector for the latter's evolutionary suppression. Increasing the relative impact of spiteful defection on a population lowers the range of evolutionary stability for TFT. When individuals participate in multiple dyads, those participating in the greatest number of dyads are most likely to provide a vehicle for the successful invasion of defection. Within social networks, ESS conditions for TFT are thus individual specific. This logic is generalized to the context of an interated n-person Prisoner's Dilemma, providing a cooperative solution conceptually identical with TFT in the two-person game.  相似文献   
22.
Mutants of Caenorhabditis elegans having about 10% of wild-type activity of the aspartyl protease cathepsin D have been isolated by screening. Mutant homozygotes have normal growth rates and no obvious morphological or developmental abnormalities. The mutant gene (cad-1) has been mapped to the right extremity of linkage group II. Heterozygous animals (cad-1/+) show intermediate enzyme levels and animals heterozygous for chromosomal deficiencies of the right extremity of linkage group II have 50% of wild-type activity. Cathepsin D purified from a mutant strain has a lower activity per unit mass of pure enzyme. These data suggest that cad-1 is a structural gene for cathepsin D.  相似文献   
23.
Three major forms of somatostatin were isolated from pancreas of the lamprey (Petromyzon marinus). One of the two major forms is a 14-residue somatostatin (SS-14) having the sequence AGCKNFFWKTFSSC. The homologous substitution Ser for Thr in position 12 is the first example of SS-14 from vertebrate preprosomatostatin gene I having a divergent sequence. The longest form is 37 residues in length (SS-37) and has the sequence ALRAAAVAGSPQQLLPLGQRERKAGCKNFFWKTFSSC. A 34-residue form (SS-34) identical in sequence but truncated at a single Arg residue at position 3 of SS-37 was also isolated. The yields of the three forms were SS-37 (0.43 nmol/g), SS-34 (134 nmol/g), and SS-14 (51.5 nmol/g). The identification of this nested series of somatostatins suggests that prosomatostatin processing in lamprey more closely resembles that observed for procholecystokinin than that of mammalian or other piscine prosomatostatins. Somatostatin-producing cells in the lamprey pancreas were identified by immunostaining using antiserum against SS-34 and anti-serum against mammalian SS-14.  相似文献   
24.
The ability of 3 plant flavonoids (morin, myricetin and quercetin) and 4 polyphenolic acids (caffeic acid, chlorogenic acid, ellagic acid and ferulic acid) to inhibit the genotoxic effects of a number of cooked-food mutagens (IQ, MeIQ, MeIQx, Trp-P-1 and Trp-P-2), was investigated in a bacterial mutation assay using Salmonella typhimurium TA98 as indicator and hepatic S9 mixes from either SWR mice or Syrian hamster as metabolic activating systems. Although the polyphenolic acids failed to have an effect, the flavonoids generally inhibited IQ, MeIQ, MeIQx and Trp-P-1 induced mutagenesis in a dose-dependent manner, irrespective of the source of S9. This was not the case with Trp-P-2 where the flavonoids were only observed to inhibit when SWR mouse S9 but not Syrian hamster S9 was used. Of the 3 compounds, myricetin and quercetin were superior to morin in their inhibitory capacity.  相似文献   
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26.
Yellowfin bream, Acanthopagrus australis , of all age classes were collected from Moreton Bay, Australia. The species possessed typical sparid ovotestes in which the testis and ovary occur in separate zones. During the spawning period (June-August) juveniles, functional males and functional females could be distinguished by the macroscopic appearance of the gonad. The sex ratio of males to females decreases with age, indicating protandrous sex inversion.
Histological and structural study of the ovotestis showed all fish have previtellogenic cells in the ovarian zone but only juvenile and male fish have developing spermatogenic cells in the testis. Most juveniles become functional males by the age of two years but a small proportion of juveniles develop directly into functional females (primary females). Protandrous sex inversion commences after the spawning period when male fish appear with spermatozoa and no other spermatogenic cells in the testis. During the period November-January male fish with no spermatogenic cells are common and a reduction in size of the testis occurs so that by March-April the ovotestis becomes structurally and histologically similar to the female ovotestis. Some fish remain functional males during their whole life-history (primary males). In functional females vitellogenic cells are present in the ovary only during the spawning period and the testis remains very small in size.  相似文献   
27.
The ability of hepatic S9 mixes derived from different rodent species (rat, mouse, Syrian and Chinese hamster) to activate the mutagens 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) and 2-amino-3,4-dimethylimidazo[4,5-f]quinoline (MeIQ) was investigated using Salmonella typhimurium strain TA98. In general, the mutagenicity of IQ and MeIQ was greatest in the presence of S9 fractions from Swiss albino mice and least from fractions derived from Chinese hamsters. However, treatment of rats or hamsters with Aroclor 1254 had little or no effect on the activation of IQ or MeIQ to mutagens.  相似文献   
28.
29.
Plutonium is not uniformly distributed in testicular tissues; thus some cell populations may receive larger or smaller radiation exposures than would be expected if the nuclide were uniformly distributed. The distributions of cell populations within alpha-particle range of Pu deposits in rat and beagle testes were determined. The data were collected from autoradiographs of testicular tissues containing 241Pu. A cell distribution factor (CDF) was determined for each cell population and is defined as the average number of each cell type within alpha-particle range of each observed Pu deposit relative to the number of each cell type that would be expected within alpha-particle range of each Pu deposit, if the deposits were distributed uniformly. In addition, the percentage of the spermatogonial stem cell population within alpha-particle range of Pu deposits was determined. In rats, the CDF for the spermatogonial stem cells is about 2.2. This value is similar to other enhancement and inhomogeneity factors reported for rodents in the literature. In beagles the CDFs to all cells in the seminiferous epithelium were less than the rats. In addition, the percentage of spermatogonial cells within alpha-particle range of Pu concentrations in the interstitial tissues was a factor of about 3 less in the dog than in the rat. The largest CDFs seen in both species were in the interstitial tissues, particularly for Leydig cells. Because the organization of testicular tissues in the beagle is quite different from rodents but more similar to human, the results from this study suggest that extrapolations from rodents to humans may tend to overestimate the potential for radiation exposure to spermatogonial stem cells as well as the fraction of the spermatogonial stem cell population at risk to exposure from internally deposited 239Pu.  相似文献   
30.
Mutations at the trkB and trkC loci of Escherichia coli produce an abnormal efflux of K+. The mutations are partially dominant in diploids and revert frequently by what appears to be intragenic suppression to the null state. The mutations can be reverted by insertion of Tn10 into the mutated gene, and spontaneous revertants are fully recessive to the mutant allele in diploids. K+ efflux produced by NEM* and by DNP* persists in strains with presumed null mutations at either locus, indicating neither gene product is the primary target for the effect of these inhibitors on K+ efflux. The results are consistent with the view that trkB and trkC encode independent systems for K+ efflux. Mutations at these loci alter regulation of the process so that K+ efflux occurs inappropriately. A second mutation to the null state abolishes this abnormal K+ efflux. These genes may encode K+/H+ antiporters, an activity postulated to mediate K+ efflux and demonstrated to exist in E. coli and other bacteria.  相似文献   
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