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Wendy M Milne 《Australian Journal of Entomology》1999,38(2):145-147
The aphid parasitoid Aphidius ervi was released in the major lucerne-growing areas of New South Wales (NSW), Australia, between 1978 and 1981. With the collaboration of district agronomists of the New South Wales Department of Agriculture, five State-wide surveys were conducted in 1982–1983 to determine the success of the release program. In each survey, the distribution of the parasitoid was checked in relation to populations of the aphids Acyrthosiphon kondoi Shinji and Acyrthosiphon pisum (Harris) (Hemiptera: Aphididae). The surveys confirmed the successful dispersal and establishment of A. ervi in the major lucerne-growing areas of NSW. They demonstrated its ability to survive and recover rapidly after a severe and widespread drought. 相似文献
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Aerosol bolus inspirations were used to assess lung injury in 15 isolated dog lungs exposed to low (0-375 units) or high doses (600-1,200 units) of papain. Effective air space size (EAD) was determined from aerosol deposition during a 5-s breath hold. Convective mixing was assessed by the spreading of the expired bolus with respect to expired volume, quantified by a coefficient of dispersion (CD) equal to the square root of the difference in the variances of the expired and inspired boluses divided by the volumetric penetration of the bolus. After exposure, CD measured with deeply penetrating boluses increased by an average of 2.5% in the low-exposure group (P greater than 0.05) and 28.0% in the high-exposure group (P less than 0.0001). CD measured with shallowly penetrating boluses decreased by 4.3% (P less than 0.0001) in the low-exposure group and increased by an average of 18.3% in the high-exposure group (P less than 0.05). Papain exposure caused EAD to increase in some lungs and decrease in others. For deep bolus penetrations, EAD changed by an average of -0.8% in the low-exposure group (P greater than 0.05) and +21.1% in the high-exposure group (P greater than 0.05). Both EAD and CD appeared to be sensitive to lung injury. However, changes in EAD were less consistent than those in CD, possibly due to changes caused by lung injury in the regional distribution of inspired aerosol. 相似文献
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Caroline van Haaften-Day Peter Russell Susan Carr Lesley Wright 《In vitro cellular & developmental biology. Plant》1988,24(10):965-971
Summary A cell line derived from a human ovarian carcinosarcoma was established in tissue culture and in nude mice. Two sublines,
LDF and HDF, separated by discontinuous density centrifugation were also established from the parent line JoN. The cloning
efficiency of the JoN line was 21%. Morphologic features of adenocarcinoma cells characteristic of the parent JoN cells were
retained in the sublines and clones; all lines showed the same karyotype and DNA content (pseudodiploid and pseudotetraploid).
Keratin, as demonstrated immunohistochemically, was strongly expressed in the parent line JoN and the xenograft tumor, but
not at all in the LDF sublines and only moderately in the HDF sublines. Vimentin, however, was expressed in neither the parent
line JoN nor the xenograft tumor, but was present in both sublines. Transglutaminase and plasminogen activator activity was
high in the parent line JoN. Neither, sublines nor clones showed the same high enzyme activity as the parent line. It is concluded
that this human tumor line JoN is comprised of epithelial cells, capable of multidirectional differentiation. 相似文献
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C.S. Holladay R.M. Wright B.L. Spangelo 《Prostaglandins, leukotrienes, and essential fatty acids》1993,49(6)
Interleukin-6 (IL-6) is a cytokine involved in the differentiation of B-cells to antibody secreting plasma cells, the activation of T-cells, and the stimulation of hepatocyte production of acute phase proteins. Because of the pro-inflammatory effects of this cytokine, we investigated the ability of the fatty acid arachidonic acid (AA) to regulate the release of IL-6 from rat resident peritoneal macrophages (Mø) in vitro. AA (0.5–16 μM) stimulated IL-6 release during a 4 h incubation period in a biphasic manner, with 4 μM AA generating a peak of IL-6 release (3-5-fold). AA (0.5–16 μM) also induced an increasing release of the AA metabolite thromboxane B2 (TXB2). The AA-induced release of IL-6 occurred within 1–2 h of incubation, whereas TXB2 concentrations were elevated within 5 min of AA treatment. The TX synthetase inhibitor CGS 12970 (4.0 μM and 40.0 μM) effectively blocked the generation of TXB2, but increased prostacyclin (PGI2) generation and potentiated the release of IL-6. In addition, PGI2, as well as the PGI2 agonists iloprost and cicaprost, stimulated IL-6 release from Mø by greater than 5-fold over vehicle-treated basal levels. These data suggest that PGI2 (but not TXA2) is involved in AA-induced IL-6 release from peritoneal Mø. 相似文献