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101.
Thirteen new congenic lines have been produced which have chromosome-7 segments introduced from different strains onto the C57BL/10Sn background. Sublines B10.P(61NX)C,D, and E received chromosome-7 segments from P/J, B10.CE(62NX) from CE/J, B10.SEC(64NX)A,C,E, and F from SEC/1Re, B10.SM(65NX) from SM/J, B10.WB(66NX) from WB/Re, B10.A(67NX) from A/SnGrf, B10.AKR(68NX) from AKR/SnGrf, and B10.K(69NX) from C3H.K. Isograft testing indicated that three sublines, B10.P(61NX)D, B10.CE(62NX)B, and B10.WB(66NX)B are histoisogenic, i.e., histocompatible within each line. With the exception of B10.A(67NX), B10.AK(68NX), and B10.K(69NX), which have not been isografted, the remaining sublines showed residual heterozygosity on isografting. The three histoisogenic lines have undergone F1 testing and have been found to possess theH-4
a
allele and new and distinct alleles at theH-1 locus. They have been designated B10.P(61NX)-H-4a
H-1
d
, B10.WB(66NX)-H-4a
H-1
e
, and B10.CE(62NX)-H-4a
H-1
f
. Direct exchange of grafts has indicated the following genotypes: B10.A(67NX)-H-4a
H-1
b
, B10.AK(68NX)-H-4a
H-1
b
, and B10.K(69NX)-F-4a
H-1
b
. The B10.SEC(64NX) and B10.SM(65NX) sublines have not been typed completely forH-4 andH-1. F
1
testing or direct exchange of skin grafts indicated that B10.P(61NX)-H-4a
H-1
d
, B10.WB(66NX)-H-4a
H-1
e
, B10.A(67NX)-H-4a
H-1
b
B10.AK(68NX)-H-4a
H-1
b
and B10.K(69NX)-H-4a
H1
b
possess nonon-H-1 histocompatibility differences from the G57BL/10 background. 相似文献
102.
103.
The role of heme in erythroid development is investigated in erythroleukemic (Friend) cells. Exogenous hemin induces the accumulation of globin mRNA and globin protein in T3-Cl2 erythroleukemia cells to levels comparable to those induced by polar solvents, such as dimethylsulfoxide (DMSO). The hemin concentration required for maximal induction (10?4 M) is the same as that which stimulates globin message translation in reticulocytes or cell-free reticulocyte lysates. Hemin and DMSO together cause T3-Cl2 cells to accumulate 8–9 fold more globin mRNA than either inducer individually. The kinetics of globin mRNA induction in hemin as compared to DMSO are very different: globin message accumulation begins 4 hr after hemin addition, but not until 30–40 hr after DMSO addition. Biliverdin induces 20–40 fold less hemoglobin than hemin; delta-aminolevulinic acid and porphobilinogen do not induce. 相似文献
104.
Development of an isoimmune serum capable of identifying a specific leukocyte antigen in the marmoset, Saguinus fuscicollis illigeri, permitted detection of lymphoid cell chimerism in this species by the cytotoxic test. This reagent was then used to identify the cell population in the chimera responsible for antibody production against a test antigen, sheep red blood cells. Primary in vitro antibody formation as measured by plaque-forming cells with blood leukocytes or splenic lymphocytes of six animals chimeric for the leukocyte antigen, MLA-1, revealed an immune response by both cell types of the chimeric population from three animals and a response by only one cell type in the other three. 相似文献
105.
106.
Pathogenic Yersiniae adhere to and kill macrophages by targeting some of their Yop proteins into the eukaryotic cytosol. There is debate about whether YopE targeting proceeds as a direct translocation of polypeptide between cells or in two distinct steps, each requiring specific signals for YopE secretion across the bacterial envelope and for translocation into the eukaryotic cytosol. Here, we used the selective solubilization of the eukaryotic plasma membrane with digitonin to measure Yop targeting during Yersinia infections of HeLa cells. YopE, YopH, YopM and YopN were found in the eukaryotic cytosol but not in the extracellular medium. When bound to SycE chaperone in the Yersinia cytoplasm, YopE residues 1–100 are necessary and sufficient for the targeting of hybrid neomycin phosphotransferase. Electron microscopic analysis failed to detect an extracellular intermediate of YopE targeting, suggesting a one-step translocation mechanism. 相似文献
107.
Francis J. Castellino Zhong Liang Patrick K. Davis Rashna D. Balsara Harsha Musunuru Deborah L. Donahue Denise L. Smith Mayra J. Sandoval-Cooper Victoria A. Ploplis Mark Walsh 《PloS one》2012,7(12)
To delineate the critical features of platelets required for formation and stability of thrombi, thromboelastography and platelet aggregation measurements were employed on whole blood of normal patients and of those with Bernard-Soulier Syndrome (BSS) and Glanzmann’s Thrombasthenia (GT). We found that separation of platelet activation, as assessed by platelet aggregation, from that needed to form viscoelastic stable whole blood thrombi, occurred. In normal human blood, ristocetin and collagen aggregated platelets, but did not induce strong viscoelastic thrombi. However, ADP, arachidonic acid, thrombin, and protease-activated-receptor-1 and -4 agonists, stimulated both processes. During this study, we identified the genetic basis of a very rare double heterozygous GP1b deficiency in a BSS patient, along with a new homozygous GP1b inactivating mutation in another BSS patient. In BSS whole blood, ADP responsiveness, as measured by thrombus strength, was diminished, while ADP-induced platelet aggregation was normal. Further, the platelets of 3 additional GT patients showed very weak whole blood platelet aggregation toward the above agonists and provided whole blood thrombi of very low viscoelastic strength. These results indicate that measurements of platelet counts and platelet aggregability do not necessarily correlate with generation of stable thrombi, a potentially significant feature in patient clinical outcomes. 相似文献
108.
109.
110.