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91.
Various process alternatives and designs of using a filter containing cellular adsorbents to remove trace viral contaminants from blood and other protein solutions have been studied. Sterilization charts have been developed that can be used to estimate the filter size required to achieve a desired sterilization criterion. A parametric study was carried out to identify various process parameters that may affect this physical trace removal process. It has been demonstrated that the adsorption rate constant is a critical parameter in the design of an efficient cellular filter for viral contaminant removal. This constant is characteristic of the virus-cell system under consideration and is shown to be particularly sensitive to the cell surface receptor density, adsorbent diameter, and fluid flow rate. Higher log titer reduction in virus concentrations can be achieved with low flow rates and no recycle. Preliminary analyses indicate the feasibility of using a magnetically stabilized fluidized filter (MSFF) reactor design for effective virus removal from these complex solutions. 相似文献
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In Escherichia coli-induced brain inflammation, cyclooxygenase-2 was induced not only on brain arterioles at 3 h, but also on infiltrating neutrophils at 9 h post-intracerebral injection. Intravenous injection of E. coli or recombinant TNFalpha also induced cyclooxygenase-2 expression on arterioles. Cyclooxygenase-2 and TNFalpha were co-localized on the arterioles as well as the infiltrating neutrophils by serial-section staining, indicating that cyclooxygenase-2 was induced by TNFalpha. NS398 (a cyclooxygenase-2 selective inhibitor) not only inhibited the increase of blood-brain barrier permeability, but also enhanced the apoptosis of the infiltrating neutrophils after E. coli stimulation. This suggests that TNFalpha-stimulated cyclooxygenase-2 induction play an important role on E. coli-induced brain inflammation. Its inhibition would help the resolution of neutrophil-mediated brain inflammation. 相似文献
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The effect of forskolin on 5-hydroxytryptamine (5-HT)-induced inositol phosphate (IP) and Ca2+ mobilisation was investigated in canine cultured aorta smooth muscle cells (ASMCs). Pretreatment of ASMCs with forskolin attenuated 5-HT-induced IP accumulation and Ca2+ mobilisation in a time- and concentration-dependent manner. The half-maximal effects (pEC50) of forskolin to attenuate IP and Ca2+ responses to 5-HT occurred at concentrations of 6.28 and 6.64, respectively. Pretreatment of ASMCs with cholera toxin caused a similar inhibition on 5-HT-induced responses. Even after treatment with forskolin for 24 h, the 5-HT-induced responses were still inhibited. The inhibitory effect of forskolin resulted from both a depression of the maximal response and a shift to the right of the concentration-effect curves of 5-HT in these responses. The water-soluble forskolin analogue L-858051 [7-deacetyl-7beta-(gamma-N-methylpiperazino)-butyryl forskolin] significantly inhibited the 5-HT-stimulated IP accumulation. In contrast, the addition of 1,9-dideoxy forskolin, an inactive forskolin analogue, had little effect on IP response. Moreover, SQ-22536 [9-(tetrahydro-2-furanyl)-9-H-purin-6-amine], an inhibitor of adenylate cyclase, and both H-89 [N-(2-aminoethyl)-5-iosquinolinesulphonamide] and HA-1004 [N-(2-guanidinoethyl)-5-iosquinolinesulphonamide], inhibitors of cAMP-dependent protein kinase (PKA), attenuated the ability of forskolin to inhibit the 5-HT-stimulated accumulation of IP in ASMCs. These results indicate that activation of cAMP/PKA might inhibit the 5-HT-stimulated IP accumulation and consequently reduce Ca2+ mobilisation, or inhibit both responses independently. 相似文献
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Chia-Hsiang Hsueh Wen-Pin Chen Jiunn-Lee Lin Chia-Ti Tsai Yen-Bin Liu Jyh-Ming Juang Hsuan-Ming Tsao Ming-Jai Su Ling-Ping Lai 《Journal of biomedical science》2009,16(1):23
The Brugada syndrome is characterized by ST segment elevation in the right precodial leads V1-V3 on surface ECG accompanied
by episodes of ventricular fibrillation causing syncope or even sudden death. The molecular and cellular mechanisms that lead
to Brugada syndrome are not yet completely understood. However, SCN5A is the most well known responsible gene that causes
Brugada syndrome. Until now, more than a hundred mutations in SCN5A responsible for Brugada syndrome have been described.
Functional studies of some of the mutations have been performed and show that a reduction of human cardiac sodium current
accounts for the pathogenesis of Brugada syndrome. Here we reported three novel SCN5A mutations identified in patients with
Brugada syndrome in Taiwan (p.I848fs, p.R965C, and p.1876insM). Their electrophysiological properties were altered by patch
clamp analysis. The p.I848fs mutant generated no sodium current. The p.R965C and p.1876insM mutants produced channels with
steady state inactivation shifted to a more negative potential (9.4 mV and 8.5 mV respectively), and slower recovery from
inactivation. Besides, the steady state activation of p.1876insM was altered and was shifted to a more positive potential
(7.69 mV). In conclusion, the SCN5A channel defect related to Brugada syndrome might be diverse but all resulted in a decrease
of sodium current. 相似文献