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161.
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Rapid identification of lettuce seed germination mutants by bulked segregant analysis and whole genome sequencing 总被引:1,自引:0,他引:1 下载免费PDF全文
Heqiang Huo Isabelle M. Henry Eric R. Coppoolse Miriam Verhoef‐Post Johan W. Schut Han de Rooij Aat Vogelaar Ronny V.L. Joosen Leo Woudenberg Luca Comai Kent J. Bradford 《The Plant journal : for cell and molecular biology》2016,88(3):345-360
Lettuce (Lactuca sativa) seeds exhibit thermoinhibition, or failure to complete germination when imbibed at warm temperatures. Chemical mutagenesis was employed to develop lettuce lines that exhibit germination thermotolerance. Two independent thermotolerant lettuce seed mutant lines, TG01 and TG10, were generated through ethyl methanesulfonate mutagenesis. Genetic and physiological analyses indicated that these two mutations were allelic and recessive. To identify the causal gene(s), we applied bulked segregant analysis by whole genome sequencing. For each mutant, bulked DNA samples of segregating thermotolerant (mutant) seeds were sequenced and analyzed for homozygous single‐nucleotide polymorphisms. Two independent candidate mutations were identified at different physical positions in the zeaxanthin epoxidase gene (ABSCISIC ACID DEFICIENT 1/ZEAXANTHIN EPOXIDASE, or ABA1/ZEP) in TG01 and TG10. The mutation in TG01 caused an amino acid replacement, whereas the mutation in TG10 resulted in alternative mRNA splicing. Endogenous abscisic acid contents were reduced in both mutants, and expression of the ABA1 gene from wild‐type lettuce under its own promoter fully complemented the TG01 mutant. Conventional genetic mapping confirmed that the causal mutations were located near the ZEP/ABA1 gene, but the bulked segregant whole genome sequencing approach more efficiently identified the specific gene responsible for the phenotype. 相似文献
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A neutral growth inhibitor, isolated from methanolic extracts of sunflower seedlings, was characterized by spectral data as caprolactam. Light-grown se 相似文献
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Selective loss of innate CD4(+) V alpha 24 natural killer T cells in human immunodeficiency virus infection 总被引:1,自引:0,他引:1
Sandberg JK Fast NM Palacios EH Fennelly G Dobroszycki J Palumbo P Wiznia A Grant RM Bhardwaj N Rosenberg MG Nixon DF 《Journal of virology》2002,76(15):7528-7534
V alpha 24 natural killer T (NKT) cells are innate immune cells involved in regulation of immune tolerance, autoimmunity, and tumor immunity. However, the effect of human immunodeficiency virus type 1 (HIV-1) infection on these cells is unknown. Here, we report that the V alpha 24 NKT cells can be subdivided into CD4(+) or CD4(-) subsets that differ in their expression of the homing receptors CD62L and CD11a. Furthermore, both CD4(+) and CD4(-) NKT cells frequently express both CXCR4 and CCR5 HIV coreceptors. We find that the numbers of NKT cells are reduced in HIV-infected subjects with uncontrolled viremia and marked CD4(+) T-cell depletion. The number of CD4(+) NKT cells is inversely correlated with HIV load, indicating depletion of this subset. In contrast, CD4(-) NKT-cell numbers are unaffected in subjects with high viral loads. HIV infection experiments in vitro show preferential depletion of CD4(+) NKT cells relative to regular CD4(+) T cells, in particular with virus that uses the CCR5 coreceptor. Thus, HIV infection causes a selective loss of CD4(+) lymph node homing (CD62L(+)) NKT cells, with consequent skewing of the NKT-cell compartment to a predominantly CD4(-) CD62L(-) phenotype. These data indicate that the key immunoregulatory NKT-cell compartment is compromised in HIV-1-infected patients. 相似文献
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Calpain-mediated Bid cleavage and calpain-independent Bak modulation: two separate pathways in cisplatin-induced apoptosis 下载免费PDF全文
Mandic A Viktorsson K Strandberg L Heiden T Hansson J Linder S Shoshan MC 《Molecular and cellular biology》2002,22(9):3003-3013
Calpain is a ubiquitous protease with potential involvement in apoptosis. We report that in human melanoma cells, cisplatin-induced calpain activation occurs early in apoptosis. Calpain activation and subsequent apoptosis were inhibited by calpeptin and PD150606, two calpain inhibitors with different modes of action. Furthermore, cisplatin induced cleavage of the BH3-only protein Bid, yielding a 14-kDa fragment similar to proapoptotic, caspase-cleaved Bid. However, Bid cleavage was inhibited by inhibitors of calpain, but not by inhibitors of caspases or of cathepsin L. Recombinant Bid was cleaved in vitro by both recombinant calpain and by lysates of cisplatin-treated cells. Cleavage was calpeptin sensitive, and the cleavage site was mapped between Gly70 and Arg71. Calpain-cleaved Bid induced cytochrome c release from isolated mitochondria. While calpeptin did not affect cisplatin-induced modulation of Bak to its proapoptotic conformation, a dominant-negative mutant of MEKK1 (dnMEKK) inhibited Bak modulation. dnMEKK did not, however, block Bid cleavage. The combination of dnMEKK and calpeptin had an additive inhibitory effect on apoptosis. In summary, calpain-mediated Bid cleavage is important in drug-induced apoptosis, and cisplatin induces at least two separate apoptotic signaling pathways resulting in Bid cleavage and Bak modulation, respectively. 相似文献
169.
Frostegård J 《Arthritis research & therapy》2011,13(3):225
During recent years atherosclerosis, the major cause of cardiovascular disease (CVD), has been recognised as a chronic inflammatory
condition in which rupture of atherosclerotic lesions appears to play a major role. The risk of CVD is raised in many rheumatic
diseases. This risk is high in systemic lupus erythematosus - as much as a 50-times increase among middle-aged women has been
reported. Studies on CVD and atherosclerosis in rheumatic disease could thus provide interesting information about CVD and
atherosclerosis in addition to being an important clinical problem. A combination of traditional and nontraditional risk factors
accounts for the increased risk of CVD and atherosclerosis in rheumatic disease. One interesting possibility is that atherosclerotic
lesions in rheumatic disease are more prone to rupture than normal atherosclerotic lesions. It is also likely that increased
risk of thrombosis may play an important role, not least in systemic lupus erythematosus. Further, it is not clear whether
an increased risk of CVD is a general feature of rheumatic disease, or whether this only occurs among subgroups of patients.
It should be emphasised that there is an apparent lack of treatment studies where CVD in rheumatic disease is the end point.
Control of disease activity and of traditional risk factors, however, appears to be well founded in relation to CVD in rheumatic
disease. Further studies are needed to determine the exact role of lipid-lowering drugs as statins. Hopefully novel therapies
can be developed that target the causes of the inflammation in atherosclerotic lesions both in rheumatic patients and in the
general population. 相似文献
170.