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761.
Sigma receptor type 1 knockout mice show a mild deficit in plasticity but no significant change in synaptic transmission in the CA1 region of the hippocampus
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Limei Chen Nicholas C. Carpita Wolf-Dieter Reiter Reginald H. Wilson Charles Jeffries Maureen C. McCann 《The Plant journal : for cell and molecular biology》1998,16(3):385-392
We have developed a rapid method to screen large numbers of mutant plants for a broad range of cell wall phenotypes using Fourier transform infrared (FTIR) microspectroscopy of leaves. We established and validated a model that can discriminate between the leaves of wild-type and a previously defined set of cell-wall mutants of Arabidopsis . Exploratory principal component analysis indicated that mutants deficient in different cell-wall sugars can be distinguished from each other. Discrimination of cell-wall mutants from wild-type was independent of variability in starch content or additional unrelated mutations that might be present in a heavily mutagenised population. We then developed an analysis of FTIR spectra of leaves obtained from over 1000 mutagenised flax plants, and selected 59 plants whose spectral variation from wild-type was significantly out of the range of a wild-type population, determined by Mahalanobis distance. Cell wall sugars from the leaves of selected putative mutants were assayed by gas chromatography-mass spectrometry and 42 showed significant differences in neutral sugar composition. The FTIR spectra indicated that six of the remaining 17 plants have altered ester or protein content. We conclude that linear discriminant analysis of FTIR spectra is a robust method to identify a broad range of structural and architectural alterations in cell walls, appearing as a consequence of developmental regulation, environmental adaptation or genetic modification. 相似文献
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McCann T. J.; Terranova G.; Keyte J. W.; Papaioannou S. S.; Mason W. T.; Meikle M. C.; McDonald F. 《American journal of physiology. Cell physiology》1998,275(1):C33
Osteoblasts can be activated by their collagen matrix and inparticular the DGEA peptide motif. We have reported that DGEA is ableto activate Ca2+ signalingpathways in the human osteoblast-like cell line, Saos-2, by a tyrosinekinase-dependent pathway (T. J. McCann, W. T. Mason, M. C. Meikle, andF. McDonald. Matrix Biol. 16:271-280, 1997). In the present study, we show that this activityis due to coupling of the signal to intracellularCa2+ stores, since the DGEA actionis not blocked by La3+ but is lostwhen Ca2+ stores are depleted with2 µM and blocked by 10 µM ryanodine. The activated stores alsodiffer functionally from those activated by thrombin, as blockade withU-73122 obstructs only thrombin-activated Ca2+ release. We have shown thatthe DGEA activity was not due to its high-charge density, since the twoacidic residues can be substituted with their uncharged homologues(asparagine and glutamine) without significant loss of activity. Thiswas in turn measured by an adhesion assay that also demonstrated thislevel of specificity. Furthermore, by constructing DGEA bound to FITC,we have shown that DGEA binding was dependent on divalent cations. Wehave also demonstrated that an intact actin cytoskeleton is notrequired for Ca2+ activation byinhibiting actin polymerization with the addition of cytochalasin B. These data strengthen the argument that collagen has a significant rolein regulating osteoblast function via this peptide motif. 相似文献
766.
Unanesthetized male rats with indwellinh right atrial cannulae were injected with morphine (MOR) i.v. which produced a dose-related increase in plasma prolactin levels (PRL). This effect was blocked partially by naloxone (NAL) at a dose of 0.06 mg/kg and totally by 0.6 mg/kg NAL. Interruption of central serotonergic neurotransmission by receptor blockade, with metergoline (MET) or cyproheptadine (Cypro), inhibition of tryptophan hydroxylase by para-chlorophenylalanine or destruction of serotonin neurons by 5, 7-dihydroxytryptamine antagonized the morphine (3 mg/kg) induced elevation in PRL release. Depression of dopaminergic activity with α-methyl-para-tyrosine elevated the basal PRL levels, but it did not prevent a further increase of prolactin levels by morphine (3 mg/kg). These data are compatible with the hypothesis that morphine stimulates PRL release by activation of the central serotonergic system. 相似文献
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It is known that PGE2 is a potent stimulus of LH release. To determine if the effect of PGE2 could be enhanced and/or prolonged by retarding its metabolic degradation, a derivative, 15-methyl PGE2 (15-E2) which is more slowly degraded than the natural compound was injected intravenously (i.v.) at various dose levels or into the third ventricle (3rd V) of ether-anesthetized, ovariectomized, estrogen (OVX, Eb)-treated rats and its effect on gonadotropin release was compared with that of PGE2. Both PGs injected i.v. were equally effective in increasing plasma LH and maintaining the elevated levels, although 15-E2 induced a larger and more sustained increase in plasma FSH than PGE2. By contrast, 3rd V PGE2 was clearly more effective than 3rd V 15-E2 in releasing LH and to a lesser extent, FSH. The effect of 15-E2 on LH was similar to that produced by 3rd V PGE1 injected at a similar dose. However, its effect on FSH was greater than that of PGE1.To evaluate the effect(s) of prostaglandins of the A and B series on gonadotropin release, PGA1, PGA2, PGB1 or PGB2 were injected intraventricularly in OVX, Eb-treated rats. PGBs were injected into conscious, free-moving rats. PGA2 or PGB2 increased plasma LH concnetrations although much less effectively than PGE2. Third V PGA1 or PGB1 were ineffective. The 3rd V injection of two cyclic esters (U-44069 and U-46619), stable analogs of the PG endoperoxide PGG2 and PGH2, induced a small, transient increase in LH levels and did not alter plasma FSH in conscious, free-moving animals. PGE2 injected intraventricularly at a similar dose was demonstrated to be much more potent than the analogs in stimulating LH and FSH release. The results indicate that: 1) 15-E2, in spite of its described long-lasting activity, does not appear to be more potent than the natural compound in releasing LH, although when injected i.v., it appeared to induce a more sustained increase in plasma FSH; 2) although PGA2 and PGB2 can also act centrally to stimulate LH release, their low potency suggests that this is a pharmacological effect; and 3) the two analogs of PG endoperoxides tested proved to be poor stimuli for gonadotropin release. The significance of these findings is discussed. 相似文献
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