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181.
MORAIS PAULO AMORIM ANTÓNIO VIEIRA DA SILVA CLÁUDIA RIBEIRO TERESA COSTA SANTOS JORGE AFONSO COSTA HELOÍSA 《Journal of genetics》2015,94(3):509-512
Journal of Genetics - 相似文献
182.
Production of sweetpotatoes, Ipomoea batatas (L.) Lam. (Convolvulaceae), is limited by several insect pests, including Diabrotica spp. (Coleoptera: Chrysomelidae), and new integrated pest management (IPM) techniques for this crop are needed. Host plant resistance is one attractive approach that fits well into IPM programs. A host plant resistance research program typically depends on reliable bioassay procedures to streamline evaluation of germplasm. Thus, a bioassay technique was developed for evaluating sweetpotato germplasm by using adults of the banded cucumber beetle, Diabrotica balteata LeConte, and spotted cucumber beetle, Diabrotica undecimpunctata howardi Barber. A single beetle was placed on a piece of sweetpotato peel (periderm and cortex with stele removed) that was embedded periderm-side up in plaster in a petri dish. Feeding and longevity of insects on 30 sweetpotato genotypes were evaluated in two experiments by using this procedure. Adult longevity ranged from 7 to 11 d for starved individuals to 211 d for beetles fed a dry artificial diet. Longevity of banded cucumber beetles that fed on sweetpotato peels ranged from 12 d for the most-resistant genotype to 123 d for SC1149-19, a susceptible control cultivar. Longevity of spotted cucumber beetles was slightly shorter than longevity of banded cucumber beetles. For the most resistant sweetpotato genotypes, both Diabrotica species exhibited a significant delay in initiation of feeding, and more beetles died on these genotypes before they had fed. Both antibiosis and nonpreference (antixenosis) are important mechanisms of resistance in sweetpotato genotypes. This bioassay was consistent with field results, indicating that this technique could be useful for evaluating resistance to Diabrotica spp. in sweetpotato genotypes. 相似文献
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184.
Gurung S Mamidi S Bonman JM Jackson EW del Río LE Acevedo M Mergoum M Adhikari TB 《TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik》2011,123(6):1029-1041
Tan spot, caused by Pyrenophora tritici-repentis, is a major foliar disease of wheat worldwide. Host plant resistance is the best strategy to manage this disease. Traditionally,
bi-parental mapping populations have been used to identify and map quantitative trait loci (QTL) affecting tan spot resistance
in wheat. The association mapping (AM) could be an alternative approach to identify QTL based on linkage disequilibrium (LD)
within a diverse germplasm set. In this study, we assessed resistance to P. tritici-repentis races 1 and 5 in 567 spring wheat landraces from the USDA-ARS National Small Grains Collection (NSGC). Using 832 diversity
array technology (DArT) markers, QTL for resistance to P. tritici-repentis races 1 and 5 were identified. A linear model with principal components suggests that at least seven and three DArT markers
were significantly associated with resistance to P. tritici-repentis races 1 and 5, respectively. The DArT markers associated with resistance to race 1 were detected on chromosomes 1D, 2A, 2B,
2D, 4A, 5B, and 7D and explained 1.3–3.1% of the phenotypic variance, while markers associated with resistance to race 5 were
distributed on 2D, 6A and 7D, and explained 2.2–5.9% of the phenotypic variance. Some of the genomic regions identified in
this study correspond to previously identified loci responsible for resistance to P. tritici-repentis, offering validation for our AM approach. Other regions identified were novel and could possess genes useful for resistance
breeding. Some DArT markers associated with resistance to race 1 also were localized in the same regions of wheat chromosomes
where QTL for resistance to yellow rust, leaf rust and powdery mildew, have been mapped previously. This study demonstrates
that AM can be a useful approach to identify and map novel genomic regions involved in resistance to P. tritici-repentis. 相似文献
185.
Verrier JD Exo JL Jackson TC Ren J Gillespie DG Dubey RK Kochanek PM Jackson EK 《Journal of neurochemistry》2011,118(6):979-987
Many organs express the extracellular 3',5'-cAMP-adenosine pathway (conversion of extracellular 3',5'-cAMP to 5'-AMP and 5'-AMP to adenosine). Some organs release 2',3'-cAMP (isomer of 3',5'-cAMP) and convert extracellular 2',3'-cAMP to 2'- and 3'-AMP and convert these AMPs to adenosine (extracellular 2',3'-cAMP-adenosine pathway). As astrocytes and microglia are important participants in the response to brain injury and adenosine is an endogenous neuroprotectant, we investigated whether these extracellular cAMP-adenosine pathways exist in these cell types. 2',3'-, 3',5'-cAMP, 5'-, 3'-, and 2'-AMP were incubated with mouse primary astrocytes or primary microglia for 1 h and purine metabolites were measured in the medium by mass spectrometry. There was little evidence of a 3',5'-cAMP-adenosine pathway in either astrocytes or microglia. In contrast, both cell types converted 2',3'-cAMP to 2'- and 3'-AMP (with 2'-AMP being the predominant product). Although both cell types converted 2'- and 3'-AMP to adenosine, microglia were five- and sevenfold, respectively, more efficient than astrocytes in this regard. Inhibitor studies indicated that the conversion of 2',3'-cAMP to 2'-AMP was mediated by a different ecto-enzyme than that involved in the metabolism of 2',3'-cAMP to 3'-AMP and that although CD73 mediates the conversion of 5'-AMP to adenosine, an alternative ecto-enzyme metabolizes 2'- or 3'-AMP to adenosine. 相似文献
186.
In cystic fibrosis (CF), bacteria of the Burkholderia cepacia complex (Bcc) can induce a fulminant inflammation with pneumonitis and sepsis. Lipopolysaccharide (LPS) may be an important virulence factor associated with this decline but little is known about the molecular pathogenesis of Bcc LPS. In this study we have investigated the inflammatory response to highly purified LPS from different Bcc clinical isolates and the cellular signalling pathways employed. The inflammatory response (TNFalpha, IL-6) was measured in human MonoMac 6 monocytes and inhibition experiments were used to investigate the Toll-like receptors and associated adaptor molecules and pathways utilized. LPS from all clinical Bcc isolates induced significant pro-inflammatory cytokines and utilized TLR4 and CD14 to mediate activation of mitogen-activated protein kinase pathways, IkappaB-alpha degradation and NFkappaB activation. However, LPS from different clinical isolates of the same clonal strain of Burkholderia cenocepacia were found to induce a varied inflammatory response. LPS from clinical isolates of Burkholderia multivorans was found to activate the inflammatory response via MyD88-independent pathways. This study suggests that LPS alone from clinical isolates of Bcc is an important virulence factor in CF and utilizes TLR4-mediated signalling pathways to induce a significant inflammatory response. 相似文献
187.
Wallis EJ Ramsay LE Ul Haq I Ghahramani P Jackson PR Rowland-Yeo K Yeo WW 《BMJ (Clinical research ed.)》2000,320(7236):671-676
ObjectiveTo examine the accuracy of a new version of the Sheffield table designed to aid decisions on lipids screening and detect thresholds for risk of coronary heart disease needed to implement current guidelines for primary prevention of cardiovascular disease.DesignComparison of decisions made on the basis of the table with absolute risk of coronary heart disease or cardiovascular disease calculated by the Framingham risk function. The decisions related to statin treatment when coronary risk is ⩾30% over 10 years; aspirin treatment when the risk is ⩾15% over 10 years; and the treatment of mild hypertension when the cardiovascular risk is ⩾20% over 10 years.SettingThe table is designed for use in general practice.SubjectsRandom sample of 1000 people aged 35-64 years from the 1995 Scottish health survey.Results13% of people had a coronary risk of ⩾15%, and 2.2% a risk of ⩾30%, over 10 years. 22% had mild hypertension (systolic blood pressure 140-159 mm Hg). The table indicated lipids screening for everyone with a coronary risk of ⩾15% over 10 years, for 95% of people with a ratio of total cholesterol to high density lipoprotein cholesterol of ⩾8.0, but for <50% with a coronary risk of <5% over 10 years. Sensitivity and specificity were 97% and 95% respectively for a coronary risk of ⩾15% over 10 years; 82% and 99% for a coronary risk of ⩾30% over 10 years; and 88% and 90% for a cardiovascular risk of ⩾20% over 10 years in mild hypertension.ConclusionThe table identifies all high risk people for lipids screening, reduces screening of low risk people by more than half, and ensures that treatments are prescribed appropriately to those at high risk, while avoiding inappropriate treatment of people at low risk. 相似文献
188.
189.
190.
The measurement of membrane potential during photosynthesis and during respiration in intact cells of Rhodopseudomonas capsulata by both electrochromism and by permeant ion redistribution. 总被引:3,自引:1,他引:3 下载免费PDF全文
Adenosine deaminase was purified 3038-fold to apparent homogeneity from human leukaemic granulocytes by adenosine affinity chromatography. The purified enzyme has a specific activity of 486 mumol/min per mg of protein at 35 degrees C. It exhibits a single band when subjected to sodium dodecyl sulphate/polyacrylamide-gel electrophoresis, non-denaturing polyacrylamide-gel electrophoresis and isoelectric focusing. The pI is 4.4. The enzyme is a monomeric protein of molecular weight 44000. Both electrophoretic behaviour and molecular weight differ from those of the low-molecular-weight adenosine deaminase purified from human erythrocytes. Its amino acid composition is reported. Tests with periodic acid-Schiff reagent for associated carbohydrate are negative. Of the large group of physiological compounds tested as potential effectors, none has a significant effect. The enzyme is specific for adenosine and deoxyadenosine, with Km values of 48 microM and 34 microM respectively. There are no significant differences in enzyme function on the two substrates. erythro-9-(2-Hydroxy non-3-yl) adenine is a competitive inhibitor, with Ki 15 nM. Deoxycoformycin inhibits deamination of both adenosine and deoxyadenosine, with an apparent Ki of 60-90 pM. A specific antibody was developed against the purified enzyme, and a sensitive radioimmunoassay for adenosine deaminase protein is described. 相似文献