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991.
A cytophysiological study was carried out of the functional status of a halo as a response of the host plant to contact with a powdery mildew pathogen. Interactions of the powdery mildew causative agents with barley, wheat, wheat–wheat-grass hybrids, wheat-aegilops lines, and aegilops with different genotypic resistance lead to the expression of haloes during pathogens, which are induced by infection pegs of the primary growth tubes, appressoria, and hyphal lobes. Haloes are visualized using cytochemical reactions to proteins and scanning electron microscopy. The observed differences in the size of haloes and intensity of their staining (uniform or zonal) are related, to a great extent, to individual reactions of the plant cell at the penetration site and, to a lesser extent, to the level of genotypic resistance. An analysis of electron microscopy and cytochemistry studies suggests that the halo as a physiologically active zone is localized at the level of the plant cell plasmalemma. Active taxis of the cell organelles to the site of infection during the formation of a halo suggests that some kind of informational signals to changes in the cell metabolism are spread from the halo zone, which lead to compatible or incompatible interactions.  相似文献   
992.
993.
Intracellular distribution of cytoskeleton-bound and soluble phosphofructokinase (PFK) (the rate-limiting enzyme in glycolysis) in mdx dystrophic muscle was the same as in control nondystrophic muscle. However, the allosteric activity of both bound and soluble PFK was reduced in mdx muscle, accompanied by a decrease in ATP level. In contrast to normal muscle, the cytoskeleton-bound PFK in mdx muscle was sensitive to allosteric regulation, like the soluble enzyme. This change in the properties of cytoskeletal PFK in mdx mice may result from the absence of dystrophin, believed to reside in the cytoskeleton. The findings that cytoskeletal PFK in mdx muscle, although altered, remains bound to cytoskeleton may play a role in muscle structure and function and the mild clinical symptoms in mdx mice.  相似文献   
994.
995.
996.
The equine leucocyte antigen (ELA) types and the clinical diagnosis for equine sarcoid and summer dermatitis were evaluated in 2026 horses representing five breeds. Data were analysed in unrelated animals and in family material. In the case of equine sarcoid, a strong association was observed between the ELA class II DW13 antigen and its effect on Swiss (cP < 0·001), French (cP < 0·0001) and Irish (cP < 0·01) Warmblood horses. The class I antigen A3 occurred more frequently in sarcoid-affected French horses (cP < 0·001). These results confirm our earlier findings (Gerber et al. 1988). Among Freiberger horses, which lack the ELA DW13 and A3 specificities, a breed-specific class I antigen, ABe108, displayed an increased frequency (cP < 0·05) in the affected group. Among Arabian horses, a tendency for increased frequency of the A1 antigen was observed in the affected animals, but the number of affected horses is too small for statistical significance. The Mendelian segregation in diseased half-siblings by ELA DW13 heterozygous stallions showed a strong association (P < 0·0001) between the inherited DW13 antigen and susceptibility to the sarcoid effect. In the case of summer dermatitis, previously published data (Marti et al. 1992) have been extended. The ELA types in four multiple-case families, founded by the same stallion, were analysed for an association with the effect of sarcoid. Eight out of nine ELA-typed affected offspring inherited the paternal haplotype A15, DW23 in contrast to nonaffected offspring where three out of 12 displayed these antigens (P < 0·005). Moreover, the ELA haplotypes of 11 out of 12 informative affected half-siblings sired by another stallion inherited the paternal haplotype A3, W12, DW23 (P < 0·05). Our findings demonstrate statistically significant associations between certain ELA antigens and two equine diseases. It is still unknown if the major histocompatibility complex (MHC) molecules themselves or another linked gene(s) play a role in the pathogenesis of these conditions.  相似文献   
997.
998.
The effects of ozone on Phaseolus vulgaris cv. Lit were investigatedusing open-top chambers (OTCs) ventilated with charcoal andPurafil filtered air (CF treatments), ambient air (NF treatments)and ambient air to which low, medium or high concentrationsof ozone were added (NFL, NFM and NFH). Ozone additions of 8,16 and 23 nl l–1 were made during phase 1 of the experiment(0–44 d after emergence, DAE), and additions of 15, 30and 47 nl l–1 were made during phase 2 (45–99 DAE).Ozone was added to the chambers between 1100 and 1800 h GMT,for 3 or 4 consecutive days each week. The seasonal 7-h meanozone concentrations were 8, 21, 27, 33 and 38 nl l–1in the CF, NF, NFL, NFM and NFH treatments, respectively. No visible symptoms of ozone injury or significant physiologicalchanges were detected in P. vulgaris during phase I of the experiment.In phase 2, the photosynthesis (Pn) and stomatal conductance(gs) of NFH-plants were inhibited by 73% and 86%, respectively,during ozone exposure, and recovered to pre-exposure valueson the following day. These observations were made prior tothe appearance, 60 DAE, of bronze lesions on the leaves of NFH-plants.The photosynthetic capacity and gs of NFH-leaves decreased asthe severity of ozone injury increased. Rates of weight lossfrom excised leaves also increased with increasing ozone injury.Microscopic investigations of the bronzed regions revealed extensivecellular breakdown, including tonoplast and chloroplast enveloperupture, and the aggregation of the cytoplasmic contents towardsone end of the cell. Severely damaged leaves abscised from the plants, resultingin premature canopy senescence in the NFM and NFH treatments.This, coupled with the lower photosynthetic capacity of existingleaves led to 25 % lower yield in the NFH than the NF treatment(P < 0.05). Phaseolus vulgaris, green bean, ozone, symptom development, photosynthesis, cell ultrastructure  相似文献   
999.
An assessment was made of two methods for determining the potency of tissue-type plasminogen activator (TPA). A chromogenic microtitre plate assay was established which contained TPA, plasminogen, a synthetic plasmin substrate (H-D-valyl-L-leucyl-L-lysyl-p-nitroaniline dihydrochloride, S2251) and any one of the following stimulators: native fibrinogen, enzymatic and chemical digests of fibrinogen, poly-D-lysine (PDL) and chemical derivatives of the latter. The chromogen assay was compared with an automated clot-lysis (turbidimetric) assay for sensitivity, reproducibility and validity for potency determination. Reference preparations of TPA were titrated in both assays: in the chromogen assay the dose-response curves were non-parallel, whereas parallelism was observed in the clot-lysis assay. Thus, the chromogen assay was restricted in its applicability and disqualified from any routine regulatory use. The potency of individual lots of recombinant (r)TPA could only be estimated in International Units (IU) of TPA activity with the automated clot-lysis assay and the potency values obtained (IU/vial) were in remarkably close agreement with the manufacturers' values.  相似文献   
1000.
Three types of Golgi-stained neurons were discovered in brain stem reticular nuclei of 30-day-old kittens: sparsely branching reticular neurons, those with densely branching dendritic trees, and giant multipolar neurons (Leontovich's classification). Adopting computerized morphometric techniques enabled 23 different parameters to be measured in cells of these types. The measurements taken from the neuronal groups investigated revealed statistically significant differences between them for most parameters. It was concluded from this that each of the neuronal types distinguished has its own morphological identity (or stability). Characteristics of structural differences and properties of differing cell types in reticular nuclei are discussed in relation to their functional properties.Institute of Higher Nervous Activity and Neurophysiology, Academy of Sciences of the USSR, Moscow. Translated from Neirofiziologiya, Vol. 23, No. 4, pp. 399–409, July–August, 1991.  相似文献   
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