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Endothelial cells lining the vasculature share some properties with macrophages and neutrophils in that they can take up material from the blood and are known to migrate, particularly during wound healing. We observed that endothelial cells isolated from bovine pulmonary arteries ingested magnetic iron oxide particles during culture in vitro. Using a non-optical, magnetometric method, we examined motions of magnetic-particle containing intracellular vacuoles. We demonstrated that these organelles move within endothelial cells, but at a slower rate than phagosomes within macrophages. Magnetometry was used to show that incubation with endotoxin (10 micrograms/ml) for 4 hr resulted in a decrease in cytoplasmic movement; yet the fluidity of the cytoplasm was increased, as measured by intracellular particle response to forced motion. We conclude that intracellular magnetic probe particles can detect vesicular motion in endothelial cells, and that endotoxin exposure can affect endothelial cells directly, altering their physical properties; these alterations precede ultrastructural evidence of cell death. 相似文献
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Equations have been derived that improve the quantification of sensory equidistant colour and lightness differences. This has been achieved by a physiological approach involving non-linear responses of cone mechanisms and two subsequent stages of linear opponent transformation to describe the Munsell System (Seim and Valberg, 1980). Using the formulation for the first opponent stage, colours induced into an achromatic center field by a chromatic surround varying in purity, are shown to follow the same power function of the opponent coordinates for all hues. By analogy, a physiological model for colour coding and colour induction is offered. Double opponent neurones with spatially antagonistic, spectrally opponent and symmetric receptive fields constitute the units of the model. Colour induction is related to lateral excitation and colour differences to response differences of these units. 相似文献
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K. L. Fritz M. E. McCue S. J. Valberg A. K. Rendahl J. R. Mickelson 《Animal genetics》2012,43(6):730-738
Recurrent exertional rhabdomyolysis is a heritable disorder that results in painful skeletal muscle cramping with exercise in up to 10% of all Thoroughbred racehorses. Here, we report a genome‐wide association study with 48 282 SNPs analyzed among 48 case and 37 control Thoroughbreds. The most significant SNPs spanned approximately 13 Mb on ECA16, and the P‐value of the most significant SNP after correcting for population structure was 8.0 × 10?6. This region on ECA16 was further evaluated by genotyping 247 SNPs in both the initial population and a second population of 34 case and 98 control Thoroughbreds. Several SNPs across the 13‐Mb region on ECA16 showed significance when each population was analyzed separately; however, the exact positions of the most significant SNPs within this region on ECA16 varied between populations. This variability in location may be attributed to lack of power owing to insufficient sample sizes within each population individually, or to the relative distribution of long, conserved haplotypes, characteristic of the Thoroughbred breed. Future genome‐wide association studies with additional horses would likely improve the power to resolve casual loci located on ECA16 and increase the likelihood of detecting any additional loci on other chromosomes contributing to disease susceptibility. 相似文献
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Valberg P. A.; Brain J. D.; Sneddon S. L.; LeMott S. R. 《Journal of applied physiology》1982,53(4):824-837
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Iron balance in the mouse 总被引:2,自引:0,他引:2
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