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111.
Gregory A. Moore George E. N. Kass Steven K. Duddy Geoffrey C. Farrell Juan Llopis Sten Orrenius 《Free radical research》1990,8(4):337-345
Isolated hepatocytes and the isolated perfused rat liver have been used to study the alterations of cytosolic free Ca2+ concentration ([Ca2+]i) produced by 2,5-di(tert-butyl)-l.4-benzohydroquinone (tBuBHQ), a potent inhibitor of hepatic microsomal Ca2+ sequestration (Moore. G.A., McConkey. D.J., Kass, G.E.N., OBrien, P.J. and Orrenius, S. FEBS Lett.,224, 331-336). (1987). Addition of tBuBHQ to isolated hepatocytes caused a rapid increase in [Ca2+]i which was similar in magnitude to the [Ca2+]i elevation induced by the Ca2+ mobilizing hormone, vasopressin. In contrast with vasopressin which caused a Ca2+ transient, tBuBHQ elevated [Ca2+]i to a new steady state that was maintained for up to 15-20min. When vasopressin was administered during the tBuBHQ-induced period of elevated [Ca2+]i. [Ca2+]i, rapidly returned to basal levels. Similarly, if vasopressin was administered just prior to tBuBHQ, the resultant tBuBHQ-dependent change in [Ca2+]i was transient. and not sustained. The hydroquinone mobilized the same intracellular Ca2+ pool as inositol 1,4,5-trisphosphate. but tBuBHQ did not produce any detectable inositol polyphosphate accumulation. IBuBHQ stimulated glucose release from perifused hepatocytes. mimicking the effect of vasopressin. In the perfused liver, tBuBHQ infusion produced a single, slow and prolonged release of Ca2+ into the perfusate and inhibition of subsequent vasopressin-induced Ca2+ effluxes. Inhibition of the response to vasopressin was reversed over time, and closely correlated with the extent of inhibition of both Ca2+ sequestration and (Ca2+-Mg2+)-ATPase activity in microsomes isolated from the isolated perfused liver. The present results are consistent with tBuBHQ inhibiting ATP-dependent Ca2+ sequestration by a direct effect on the endoplasmic reticular Ca2+ pump, which results in net Ca2+ release and elevation of [Ca2+]i. Furthermore. vasopressin appears to stimulate active removal of increased [Ca2+] from the hepatocyte cytosol by a mechanism which does not depend on reuptake of Ca2+ into the endoplasmic reticulum
2,5-Di(tert-butyl) -l,4-benmhydroquinone. calcium. hepatocytes. perfused liver, endoplasmic reticulum 相似文献
2,5-Di(tert-butyl) -l,4-benmhydroquinone. calcium. hepatocytes. perfused liver, endoplasmic reticulum 相似文献
112.
Maris G. N. Hartmanis Tomas Klason Sten Gatenbeck 《Applied microbiology and biotechnology》1984,20(1):66-71
Summary The pathway for uptake of acids during the solvent formation phase of an acetone-butanol fermentation by Clostridium acetobutylicum ATCC 824 was studied. 13C NMR investigations on actively metabolizing cells showed that butyrate can be taken up from the medium and quantitatively converted to butanol without accumulation of intermediates. The activities of acetate phosphotransacetylase, acetate kinase and phosphate butyryltransferase rapidly decreased to very low levels when the organism began to form solvents. This indicates that the uptake of acids does not occur via a reversal of these acid forming enzymes. No short-chain acyl-CoA synthetase activity or butyryl phosphate reducing activity could be detected. Based on our results and a critical analysis of literature data on acetone-butanol fermentations, it is suggested that an acetoacetyl-CoA: acetate (butyrate) CoA-transferase is solely responsible for uptake and activation of acetate and butyrate in C. acetobutylicum. The transferase exhibits a broad carboxylic acid specificity. The key enzyme in the uptake is acetoacetate decarboxylase, which is induced late in the fermentation and pulls the transferase reaction towards formation of acetoacetate. The major implication is that it is not feasible to obtain a batch-wise butanol fermentation without acetone formation and retention of a good yield of butanol. 相似文献
113.
The fate of ochratoxin A during incubation with contents from the four stomachs of the cow was studied. It was concluded that ochratoxin A was cleaved into the nontoxic ochratoxin α and phenylalanine by the contents from all but the abomasum. 相似文献
114.
115.
Sten Linnarsson 《Genome biology》2013,14(4):305
A report on the third Single Cell Analyses meeting, held at the Cold Spring Harbor Laboratory, New York, USA, March 6-9, 2013. 相似文献
116.
Human leucocytes were incubated in the presence of vinyl acetate or acetaldehyde (10-20 mM) for 4 h at 37 degrees C in vitro. DNA damage was analysed by alkaline elution. None of the compounds induced a detectable increase in the frequency of DNA strand breaks. Cells exposed to 5 Gy of X-ray immediately after treatment and before alkaline elution showed a clear, dose-dependent retardation of the elution rate in comparison with X-irradiated control cells. These results demonstrate that both vinyl acetate and acetaldehyde induce DNA cross-links in human cells. 相似文献
117.
Most previous models of the spinal central pattern generator (CPG) underlying locomotion in the lamprey have relied on reciprocal
inhibition between the left and right side for oscillations to be produced. Here, we have explored the consequences of using
self-oscillatory hemisegments. Within a single hemisegment, the oscillations are produced by a network of recurrently coupled
excitatory neurons (E neurons) that by themselves are not oscillatory but when coupled together through N-methyl-d-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionicacid (AMPA)/kainate transmission can produce oscillations.
The bursting mechanism relies on intracellular accumulation of calcium that activates Ca2+-dependent K+. The intracellular calcium is modeled by two different intracellular calcium pools, one of which represents the calcium entry
following the action potential, CaAP pool, and the other represents the calcium inflow through the NMDA channels, CaNMDA pool. The Ca2+-dependent K+ activated by these two calcium pools are referred to as KCaAP and KCaNMDA, respectively, and their relative conductances are modulated and increase with the background activation of the network.
When changing the background stimulation, the bursting activity in this network can be made to cover a frequency range of
0.5–5.5 Hz with reasonable burst proportions if the adaptation is modulated with the activity. When a chain of such hemisegments
are coupled together, a phase lag along the chain can be produced. The local oscillations as well as the phase lag is dependent
on the axonal conduction delay as well as the types of excitatory coupling that are assumed, i.e. AMPA/kainate and/or NMDA.
When the caudal excitatory projections are extended further than the rostral ones, and assumed to be of approximately equal
strength, this kind of network is capable of reproducing several experimental observations such as those occurring during
strychnine blockade of the left-right reciprocal inhibition. Addition of reciprocally coupled inhibitory neurons in such a
network gives rise to antiphasic activity between the left and right side, but not necessarily to any change of the frequency
if the burst proportion of the hemisegmental bursts is well below 50%. Prolongation of the C neuron projection in the rostrocaudal
direction restricts the phase lag produced by only the excitatory hemisegmental network by locking together the interburst
intervals at different levels of the spinal cord.
Received: 29 September 1998 Accepted in Revised Form: 26 March 1999 相似文献
118.
119.
Gunnar Selstam Jan Liljekvist Sten Rosberg Lena Grönquist Torsten Perklev Kurt Ahrén 《Prostaglandins & other lipid mediators》1974,6(4):303-311
Isolated whole ovaries from 23–24 day-old rats were studied in order to compare the effects of prostaglandin E1 (PGE1) and luteinizing hormone (LH) on ovarian cyclic adenosine 3′,5′-monophosphate (cAMP) production. Both substances produced a dose-dependent accumulation of cAMP in the ovarian tissue as well as in the incubation medium. The release of cAMP to the incubation medium was considerable after long periods of incubation (60–120 min). Time-relationships for LH- and PGE1-effects were different. Maximal cAMP content in the tissue after addition of PGE1 was seen already after 5–15 min of incubation whereas LH gave a maximal response after around 60 min. Accumulation of cAMP in the medium was approximately linear with time for both LH and PGE1. Addition of theophylline potentiated the action of PGE1 and LH but did not change the time-courses of the effects. It is concluded that the accumulation of cAMP in the medium should be considered in studies with various in vitro types of ovarian preparations. It is also pointed out that the different time-courses of the LH- and PGE1-effects make the interpretation of additivity experiments difficult. 相似文献
120.