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221.
Isamu Tanaka Akio Horie Joji Haratake Yasushi Kodama Kenzaburo Tsuchiya 《Biological trace element research》1988,16(1):19-26
There are few inhalation studies of nickel carcinogenesis. In this study, Wistar male rats were exposed to green nickel oxide
(NiO(G)) aerosols (mass median aerodynamic diameter, 0.6 μm) for 7 h/d, 5 d/wk for up to 12 mo. The average exposure concentration
was controlled at 0.3 and 1.2 mg/m3 during the exposure. For histopathological examination and measurement of the nickel concentration in rat organs, the rats
were sacrificed at 3, 6, and 12 mo of exposure and 8 mo clearance period following 12 mo of exposure.
The nickel content in rat lungs that was observed up to 2.6 mg after 12 mo exposure, was proportional to the exposure concentration
during the exposure. The clearance of the nickel from the lungs was very slow and the biological half time was determined
7.7 mo.
Although the rats were exposed continuously to NiO(G), for 12 mo and kept for 8 mo clearance period, there were no malignant
tumors in any of the exposed animals. 相似文献
222.
Superoxide anion (O
2
.–
) was photogenerated upon illumination of riboflavin in fluorescent light. The rate of O
2
.–
formation was stimulated by double stranded DNA but not by denatured DNA or RNA. Depurinated DNA, which was predominantly depleted in guanine residues, did not exhibit the stimulatory effect, indicating an interaction of riboflavin, or active oxygen species derived from it, with guanine bases. Also, the stimulation of O
2
.–
photogeneration was not observed with ethidium bromide but was seen with proflavin-intercalated DNA. Since ethidium bromide intercalates preferentially between purines and pyrimidines, and proflavin prefers dA-dT rich sites, these results were interpreted to suggest that the interaction of riboflavin with DNA is mainly with GC or CG base pairs. 相似文献
223.
Chromium is an essential trace element and is associated with some biological pathways, especially with glucose tolerance.
For these reasons, we decided to determine the concentration of chromium in two sets of Brazilian medicinal plants. The first
group consisted of plants that are considered as antidiabetic, whereas the second included plants that do not have this therapeutic
property. The concentration of chromium was determined by flameless atomic absorption. All the plants analyzed contain chromium
in the normal range for this element, but the hypoglycemic plants contain more chromium than the others (1–4 μg/g compared
to 0.5–1.5 μg/g). 相似文献
224.
Richard W. Joy IV Kamlesh R. Patel Trevor A. Thorpe 《Plant Cell, Tissue and Organ Culture》1988,13(3):219-228
The effect of ascorbic acid on growth and shoot formation in callus cultures of tobacco (Nicotiana tabacum L.) was investigated, using young (4–12 subcultures) and old (more than 30 subcultures) tissue. It was found that ascorbate, at levels of 4–8×10-4M, enhanced shoot formation in both young and old callus. Treatment with ascorbate also speeded up the shoot-forming process. In addition, ascorbate completely reversed the inhibition of shoot formation by gibberellic acid in young callus, but was less effective in old callus. 相似文献
225.
InRhizobium meliloti, the promoter P1 of thenif HDK operon, and also the promoter P2, have earlier been shown to be active in the bacteria present in alfalfa root nodules, but
not in the bacteria grown aerobically in culture. Here we have looked at the expression from P1 and P2 in two non-symbiotic
nitrogen-fixing bacteria,Azotobacter vinelandii andAzospirillum brasilense, using constructions in which the promoters are fused upstream of theβ-galactosidase gene. The promoter P1, but not P2, is active inA. vinelandii, while neither P1 nor P2 is active inAzospirillum brasilense. 相似文献
226.
227.
四川宝兴雉类生态和垂直分布的调查研究 总被引:2,自引:0,他引:2
宝兴位于四川盆地西缘山地,境内纵贯世界闻名的大雪山——即夹金山。 自19世纪30年代至20世纪30年代,先后有Verreaux(1838—1871),Geoffroy(1866),David(1871),Seinhoe(1871),Sharpe(1875),David et Oustalet(1877),Oustaler (1891—92),Styan(1899),Laubmann(1920),La Touch(1925—30),Smith(1931—34),Bangs(1932),Seys(1934)等对宝兴进行过调查和采集,而我 相似文献
228.
Formation of the Neurotransmitter Glycine from the Anticonvulsant Milacemide Is Mediated by Brain Monoamine Oxidase B 总被引:5,自引:1,他引:4
Philippe Janssens de Varebeke Robert Cavalier Michèle David-Remacle Moussa B. H. Youdim 《Journal of neurochemistry》1988,50(4):1011-1016
Milacemide (2-n-pentylaminoacetamide) is a secondary monoamine that in the brain is converted to glycinamide and glycine. This oxidative reaction was suspected to involve the reaction of monoamine oxidase (MAO). Using mitochondrial preparations from tissues that contain MAO-A and -B (rat brain and liver), MAO-A (human placenta), and MAO-B (human platelet and bovine adrenal chromaffin cell), it has been established that mitochondria containing MAO-B rather than MAO-A oxidize (H2O2 production and glycinamide formation) milacemide. The apparent Km (30-90 microM) for milacemide oxidation by mitochondrial MAO-B preparations is significantly lower than that for milacemide oxidation by mitochondrial MAO-A (approximately 1,300 microM). In vitro MAO-B (l-deprenyl and AGN 1135) rather than MAO-A (clorgyline) selectively inhibited the oxidation of milacemide. These in vitro data are matched by ex vivo experiments where milacemide oxidation was compared to oxidation of serotonin (MAO-A) and beta-phenylethylamine (MAO-B) by brain mitochondria prepared from rats pretreated with clorgyline (0.5-10 mg/kg) and l-deprenyl (0.5-10 mg/kg). Furthermore, in vivo experiment demonstrated that l-deprenyl selectively increased the urinary excretion of [14C]milacemide and the total radioactivity with a concomitant decrease of [14C]glycinamide. Such changes were not observed after clorgyline treatment, but were evident only at doses beyond clorgyline selectivity. The present data therefore demonstrate that milacemide is a substrate for brain MAO-B, and its conversion to glycinamide, further transformed to the inhibitory neurotransmitter, glycine, mediated by this enzyme may contribute to its pharmacological activities. 相似文献
229.
Characterization of Microtubule-Associated Protein 2 from Mouse Brain and Its Localization in the Cerebellar Cortex 总被引:3,自引:2,他引:1
Michio Niinobe Nobuaki Maeda Hidetoshi Ino Katsuhiko Mikoshiba 《Journal of neurochemistry》1988,51(4):1132-1139
Microtubule-associated protein (MAP) 2 was purified from the microtubule fraction of mouse brain by heat treatment and BioGel A-5m gel filtration. The purified preparation showed a single protein band on sodium dodecyl sulfate-polyacrylamide gel electrophoresis using both a gradient gel (3.75-12.5%) and a low-percentage gel (5%), a finding indicating that MAP2B was absent under the conditions used. Amino acid analysis revealed that mouse MAP2 was an acidic protein with an isoelectric point (pI 4.5) and amino acid composition similar to those of porcine brain MAP2. Immunoblot analysis indicated that the antigens that reacted with MAP2 antiserum were present in large quantities in mouse brain. However, we also found a weak reaction in various tissues other than brain, and the major antigens involved were recognized to be common molecular species with the same molecular mass, 162 and 170 kilodaltons. Using antiserum against mouse brain MAP2, the developmental localization patterns of MAP2 in the mouse cerebellar cortex were studied by immunohistochemistry. MAP2 was mainly localized in the neuronal cells throughout development, with the expression in Purkinje cell dendrites being especially remarkable in the growth of arborization from postnatal day 3 to day 20. At the mature stage, the reaction was strong in the dendritic tree but very weak in the proximal dendrites and cell bodies. 相似文献
230.
Jean-Paul Kan Régis Steinberg Jérome Leclercq Paul Worms Kathleen Biziere 《Journal of neurochemistry》1988,50(4):1137-1144
In rodents, SR 95191 [3-(2-morpholinoethylamino)-4-cyano-6-phenylpyridazine] has been shown to be active in animal models of depression. The profile of activity of SR 95191 suggests that the compound is a selective and short-acting type A monoamine oxidase (MAO) inhibitor (MAOI) in vivo. In the present study, the interaction of SR 95191 with MAO-A and MAO-B activity was further examined in vivo and in vitro. In brain, liver, and duodenum of pretreated rats, SR 95191 selectively inhibited MAO-A (ED50 = 3-5 mg/kg, p.o.), whereas MAO-B was only weakly inhibited for doses as high as 300 mg/kg, p.o. In vivo, SR 95191 (1-100 mg/kg, p.o.) antagonized, in a dose-dependent fashion, the irreversible inhibition of brain and liver MAO-A induced by phenelzine. Finally, dopamine and 5-hydroxytryptamine depleted from their striatal stores by tetrabenazine were able to displace SR 95191 from the active site of MAO-A. However, ex vivo, kinetic studies showed that the inhibitory effect of SR 95191 (1-10 mg/kg) towards MAO-A was noncompetitive and was unchanged after dilution or dialysis. In vitro, the inhibition of brain MAO-A, but not MAO-B, by SR 95191 was time dependent, with a 19-fold decrease in the IC50 values being observed over a 30-min incubation period (140 to 7.5 microM). At this time, the SR 95191-induced inhibition of MAO-A was not removed by repeated washings. When the reaction was started by adding the homogenate without prior preincubation with SR 95191, the inhibition of brain MAO-A was fully competitive (Ki = 68 microM).(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献