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61.
62.
Douglas H. Sandberg 《The Western journal of medicine》1961,94(5):287-291
In considering drug therapy for pregnant women, it must be borne in mind that almost all chemical compounds in use as therapeutic agents pass from the maternal to the fetal circulation through the placenta. These drugs can produce a wide range of harmful effects on the fetus and neonatal infant. The effects of some substances for which we have data reflecting a deleterious effect are listed.It is suggested that in the future more caution be exercised in using drugs during pregnancy and that in histories, both obstetrical and pediatric, any therapy given to the mother during gestation be recorded in detail. 相似文献
63.
64.
Elizabeth B. Gargus Douglas H. Robinson James K. Bubien Lawrence B. Bugaisky Dale J. Benos 《In vitro cellular & developmental biology. Plant》1989,25(5):435-441
Summary Six- and seven-day post-coitus (p.c.) rabbit embryos have been cultured in an attempt to establish a trophectodermal cell
line. Results indicate that cells with epithelial characteristics (i.e. positive staining for cytokeratin) will survive in
culture until Passage 3. At that time a fibroblastlike cell becomes predominant. In addition, we have found that the presence
of the inner cell mass is required for embryo explants often results in the development of cells that spontaneously contract.
These cells stain positively for myosin, which indicates that they may be precardiac cells. Maximum diastolic potential was
−59±1.2 mV and the threshold potential was −53±2.3 mV. Spontaneously contracting cells did not respond to atropine, acetylcholine,
epinephrine, isoproterenol, or propranolol. Action potential seems to be a result of an inward calcium current, because the
beating rate is decreased in a dose-related manner with the calcium channel blocker verapamil, whereas the voltage-sensitive
sodium channel blocker tetrodotoxin was without effect.
This work was supported by grants HD21302, HD07069, DK31091, and HL37320 from the National Institutes of Health, Bethesda,
MD, with additional support from a University of Alabama at Birmingham Cardviovascular Research and Training Center Award. 相似文献
65.
66.
67.
Jeffrey R. Bloomquist David M. Soderlund Douglas C. Knipple 《Archives of insect biochemistry and physiology》1989,10(4):293-302
Resistance to pyrethroid insecticides and dichlorodiphenyltrichloroethane (DDT) was investigated in the napts (no action potential, temperature sensitive) mutant of Drosophila melanogaster. In surface contact bioassays, the napts strain showed threefold resistance to deltamethrin at the LC50 level when compared to susceptible Canton-S flies. Cross-resistance was also observed to DDT and the pyrethroids NRDC 157 [3-phenoxybenzyl [1R,cis]-3-(2,2-dibromovinyl)-2,2-dimethylcyclopropanecarboxylate], fenfluthrin, and MTI-800 [1-(3-phenoxy-4-fluorophenyl)-4-(4-ethoxyphenyl)-4-methylpentane]. The onset of intoxication by pyrethroids in napts flies was markedly delayed, a finding that is consistent with the existence of a resistance mechanism involving reduced neuronal sensitivity. Resistance at the level of the nerve was confirmed by electrophysiological recordings of spontaneous and evoked activity in the dorsolongitudinal flight muscles of poisoned flies. Preparations from napts insects treated with fenfluthrin displayed longer latencies to the appearance of spontaneous activity and also an absence or reduction in burst discharges compared to equivalent preparations from susceptible individuals. These results are discussed in light of competing hypotheses concerning the mechanism underlying knockdown resistance and reduced nerve sensitivity in insects. 相似文献
68.
69.
Robert Y. Kanterman Christian C. Felder Douglas E. Brenneman Alice L. Ma Sandra Fitzgerald Julius Axelrod 《Journal of neurochemistry》1990,54(4):1225-1232
The alpha 1-adrenergic receptor has been shown to mediate the release of arachidonic acid in FRTL5 thyroid cells and MDCK kidney cells. In primary cultures of spinal cord cells, norepinephrine stimulated release of arachidonic acid (from neurons only) and turnover of inositol phospholipids (from neurons and glia) via alpha 1-adrenergic receptors. These two responses were dissociated by treatment with phorbol ester and pertussis toxin, which inhibited production of inositol phosphates with no appreciable effect on release of arachidonic acid. Extracellular calcium was required for release of arachidonic acid, but not for production of inositol phosphates. The calcium channel blockers nifedipine and verapamil inhibited release of arachidonic acid only. However, 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8), a compound that blocks intracellular calcium release, diminished production of inositol phosphates, but had little effect on release of arachidonic acid. These results suggest that alpha 1-adrenergic receptors couple to release of arachidonic acid in primary cultures of spinal cord cells by a mechanism independent of activation of phospholipase C, possibly via the activation of phospholipase A2. 相似文献
70.
The role of excision repair in the removal of transient benzo[a]pyrene-induced DNA lesions in Chinese hamster ovary cells 总被引:1,自引:0,他引:1
In Chinese hamster ovary (CHO) cells, benzo[a]pyrene induces both persistent and transient lesions that are detected by alkaline sucrose gradient sedimentation analysis (ASG sites). The transient lesions disappear within 15 min while the persistent lesions can be detected for several hours following treatment. Although the persistent ASG sites are believed to be repaired by excision repair, the process responsible for the disappearance of the transient ASG sites is unknown. To determine the contribution of excision repair to the removal of these transient lesions, CHO cells were treated with benzo[a]pyrene (B(a)P) in the presence of the inhibitors of excision repair, araC and novobiocin. The results indicate that: (1) araC inhibits the removal of persistent, but not the transient B(a)P-induced ASG sites; (2) novobiocin, a putative inhibitor of the incision step of DNA excision repair, reduced the number of lesions detected immediately following treatment, indicating that many of these lesions may represent single-strand discontinuities generated during repair; and (3) the lesions detected in the presence of novobiocin disappear rapidly following treatment. Based on these results, we concluded that B(a)P-induced transient ASG sites are repaired by a process other than excision repair. 相似文献