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951.
对有不良气体存在下系统的制冷热力学循环进行了分析,建立了不良气体存在时,系统循环COP的计算模型,利用所建COP模型对系统的长期性能变化进行了分析并对系统寿命进行了评估,在此基础上提出了解决系统长期性能下降问题的简便而有效的途径. 相似文献
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William Wilson Anku Samuel Osei-Bonsu Oppong Sudheesh Kumar Shukl Eric Selorm Agorku Poomani Penny Govender 《自然科学进展(英文版)》2016,26(4):354-361
This paper reports the degradation of indigo carmine and eosin Y dyes in water, catalyzed by cobalt and multiwalled carbon nanotube modified zirconium oxide nanocomposite(Co-ZrO_2-MWCNTs) under simulated visible light. The bare ZrO_2,ZrO_2-MWCNTs, Co-ZrO_2 and Co-ZrO_2-MWCNTs with different percentage compositions of cobalt were synthesized by homogeneous co-precipitation method. Characterization of the prepared nanocomposites was carried out using X-Ray powder Diffraction(XRD), Fourier Transformer Infrared(FTIR) Spectroscopy, Transmission Electron Microscopy(TEM), Raman Spectroscopy,(UV–Vis)-Spectroscopy and Energy Dispersive Spectroscopy(EDS) for their structure, formation,morphology, size and elemental analysis. The experimental results indicated that all the cobalt and MWCNTs modified nanocomposites demonstrated higher photocatalytic activities compared to the bare ZrO_2. The most efficient catalyst(0.5% Co-ZrO_2-MWCNTs) with the band gap and Ka values of 5.21 e V and 16.86*10~(-3) min~(-1) respectively exhibited 98% degradation efficiency toward indigo carmine and 87% toward eosin Y in 180 min. 相似文献
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956.
TRPML1 (mucolipin 1, also known as MCOLN1) is predicted to be an intracellular late endosomal and lysosomal ion channel protein that belongs to the mucolipin subfamily of transient receptor potential (TRP) proteins. Mutations in the human TRPML1 gene cause mucolipidosis type IV disease (ML4). ML4 patients have motor impairment, mental retardation, retinal degeneration and iron-deficiency anaemia. Because aberrant iron metabolism may cause neural and retinal degeneration, it may be a primary cause of ML4 phenotypes. In most mammalian cells, release of iron from endosomes and lysosomes after iron uptake by endocytosis of Fe(3+)-bound transferrin receptors, or after lysosomal degradation of ferritin-iron complexes and autophagic ingestion of iron-containing macromolecules, is the chief source of cellular iron. The divalent metal transporter protein DMT1 (also known as SLC11A2) is the only endosomal Fe(2+) transporter known at present and it is highly expressed in erythroid precursors. Genetic studies, however, suggest the existence of a DMT1-independent endosomal and lysosomal Fe(2+) transport protein. By measuring radiolabelled iron uptake, by monitoring the levels of cytosolic and intralysosomal iron and by directly patch-clamping the late endosomal and lysosomal membrane, here we show that TRPML1 functions as a Fe(2+) permeable channel in late endosomes and lysosomes. ML4 mutations are shown to impair the ability of TRPML1 to permeate Fe(2+) at varying degrees, which correlate well with the disease severity. A comparison of TRPML1(-/- )ML4 and control human skin fibroblasts showed a reduction in cytosolic Fe(2+) levels, an increase in intralysosomal Fe(2+) levels and an accumulation of lipofuscin-like molecules in TRPML1(-/-) cells. We propose that TRPML1 mediates a mechanism by which Fe(2+) is released from late endosomes and lysosomes. Our results indicate that impaired iron transport may contribute to both haematological and degenerative symptoms of ML4 patients. 相似文献
957.
Protein N-glycosylation requires flipping of the glycolipid Man(5)GlcNAc(2)-diphosphate dolichol (Man(5)GlcNAc(2)-PP-Dol) across the endoplasmic reticulum (ER). Helenius et al. report genetic evidence suggesting that Rft1, an essential ER membrane protein in yeast, is required directly to translocate Man(5)GlcNAc(2)-PP-Dol. We now show that a specific ER protein(s), but not Rft1, is required to flip Man(5)GlcNAc(2)-PP-Dol in reconstituted vesicles. Rft1 may have a critical accessory role in translocating Man(5)GlcNAc(2)-PP-Dol in vivo, but the Man(5)GlcNAc(2)-PP-Dol flippase itself remains to be identified. 相似文献
958.
The identification of liquid ethane in Titan's Ontario Lacus 总被引:1,自引:0,他引:1
Brown RH Soderblom LA Soderblom JM Clark RN Jaumann R Barnes JW Sotin C Buratti B Baines KH Nicholson PD 《Nature》2008,454(7204):607-610
Titan was once thought to have global oceans of light hydrocarbons on its surface, but after 40 close flybys of Titan by the Cassini spacecraft, it has become clear that no such oceans exist. There are, however, features similar to terrestrial lakes and seas, and widespread evidence for fluvial erosion, presumably driven by precipitation of liquid methane from Titan's dense, nitrogen-dominated atmosphere. Here we report infrared spectroscopic data, obtained by the Visual and Infrared Mapping Spectrometer (VIMS) on board the Cassini spacecraft, that strongly indicate that ethane, probably in liquid solution with methane, nitrogen and other low-molecular-mass hydrocarbons, is contained within Titan's Ontario Lacus. 相似文献
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Difilippantonio S Gapud E Wong N Huang CY Mahowald G Chen HT Kruhlak MJ Callen E Livak F Nussenzweig MC Sleckman BP Nussenzweig A 《Nature》2008,456(7221):529-533
Variable, diversity and joining (V(D)J) recombination and class-switch recombination use overlapping but distinct non-homologous end joining pathways to repair DNA double-strand-break intermediates. 53BP1 is a DNA-damage-response protein that is rapidly recruited to sites of chromosomal double-strand breaks, where it seems to function in a subset of ataxia telangiectasia mutated (ATM) kinase-, H2A histone family member X (H2AX, also known as H2AFX)- and mediator of DNA damage checkpoint 1 (MDC1)-dependent events. A 53BP1-dependent end-joining pathway has been described that is dispensable for V(D)J recombination but essential for class-switch recombination. Here we report a previously unrecognized defect in the joining phase of V(D)J recombination in 53BP1-deficient lymphocytes that is distinct from that found in classical non-homologous-end-joining-, H2ax-, Mdc1- and Atm-deficient mice. Absence of 53BP1 leads to impairment of distal V-DJ joining with extensive degradation of unrepaired coding ends and episomal signal joint reintegration at V(D)J junctions. This results in apoptosis, loss of T-cell receptor alpha locus integrity and lymphopenia. Further impairment of the apoptotic checkpoint causes propagation of lymphocytes that have antigen receptor breaks. These data suggest a more general role for 53BP1 in maintaining genomic stability during long-range joining of DNA breaks. 相似文献