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71.
72.
To understand the evolution of duplicate genes, we compared rates of
nucleotide substitution between 17 pairs of nonallelic duplicated genes in
the tetraploid frog Xenopus laevis with rates between the orthologous loci
of human and rodent. For all duplicated X. laevis genes, the number of
synonymous substitutions per site (dS) was greater than the number of
nonsynonymous substitutions per site (dN), indicating that these genes are
subject to purifying selection. There was also a significant positive
correlation (r = 0.915) between dN for the X. laevis genes and dN for the
mammalian genes, suggesting that, at the amino acid level, the X. laevis
genes and the mammalian genes are under similar constraints. Results of
relative-rate tests showed nearly equal rates of nonsynonymous substitution
in each copy of the X. laevis genes; apparently there are similar
constraints on both copies. No correlation was found between dS for the X.
laevis genes and dS for the mammalian genes. There was a significant
positive correlation both between members of pairs of duplicated X. laevis
genes (r = 0.951) and between human and rodent orthologues (r = 0.854) with
respect to third- position G+C content but no such relationship between the
X. laevis genes and either of their mammalian orthologues. The results
indicate that both copies of a duplicate gene can be subject to purifying
selection and thus support the hypothesis of selection against all
genotypes containing a null allele at either of two duplicate loci.
相似文献
73.
74.
Immunochemical identity of peroxisomal enoyl-CoA hydratase with the peroxisome-proliferation -associated 80,000 mol wt polypeptide in rat liver 总被引:6,自引:1,他引:5
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Peroxisome proliferators, which induce proliferation of hepatic peroxisomes, have been shown previously to cause a marked increase in an 80,000 mol wt polypeptide predominantly in the light mitochondrial and microsomal fractions of liver of rodents. We now present evidence to show that this hepatic peroxisome-proliferation-associated polypeptide, referred to as polypeptide PPA-80, is immunochemically identical with the multifunctional peroxisome protein displaying heat-labile enoyl-CoA hydratase activity. This conclusion is based on the following observations: (a) the purified polypeptide PPA-80 and the heat- labile enoyl-CoA hydratase from livers of rats treated with the peroxisome proliferators Wy-14,643 {[4-chloro-6(2,3-xylidino)-2-pyrimidinylthio]acetic acid} exhibit identical minimum molecular weights of approximately 80,000 on SDS polyacrylamide gel electrophoresis; (b) these two proteins are immunochemically identical on the basis of ouchterlony double diffusion, immunotitration, rocket immunoelectrophoresis, and crossed immunoelectrophoresis analysis; and (c) the immunoprecipitates formed by antibodies to polypeptide PPA-80 when dissociated on a sephadex G-200 column yield enoyl-CoA hydratase activity. Whether the polypeptide PPA-80 exhibits the activity of other enzyme(s) of the peroxisomal β-oxidation system such as fatty acyl-CoA oxidase activity or displays immunochemical identity with such enzymes remains to be determined. The availability of antibodies to polypeptide PPA-80 and enoyl-CoA hydratase facilitated immunofluorescent and immunocytochemical localization of the polypeptide PPA- 80 and enoyl-CoA hydratase in the rat liver. The indirect immunofluorescent studies with these antibodies provided direct visual evidence for the marked induction of polypeptide PPA-80 and enoyl-CoA hydratase in the livers of rats treated with Wy-14,643. The present studies also provide immunocytochemical evidence for the localization of polypeptide PPA- 80 and the heat-labile enoyl-CoA hydratase in the peroxisome, but not in the mitochondria, of hepatic parenchymal cells. These studies, therefore, provide morphological evidence for the existence of fatty acyl-CoA oxidizing system in peroxisomes. An increase of polypeptide PPA-80 on SDS polyacrylamide gel electrophoretic analysis of the subcellular fractions of liver of rodents treated with lipid-lowering drugs should serve as a reliable and sensitive indicator of enhanced peroxisomal β- oxidation system. 相似文献
75.
Use of polymyxin B, levallorphan, and tetracaine to isolate novel envelope mutants of Escherichia coli.
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Mutants of Escherichia coli were isolated by their resistance to the bacteriocidal effects of the membrane-active drugs polymyxin B, levallorphan, and tetracaine. The mutants were examined for additional changes in cellular physiology evoked by the lesions; many polymyxin-resistant strains had a concomitant increased sensitivity to anionic detergents, and several strains of each type had concomitant alterations in generation time and morphology. Mutants of each class (polymyxin resistant, tetracaine resistant, and levallorphan resistant) were transduced into recipient strains. The levallorphan resistance site (lev) was located at approximately 9 min on the E. coli chromosome. Polymyxin (pmx) and tetracaine (tec) resistance loci were also transduced. The lev and tec strains had a slight prolongation of generation time, in contrast with their isogenic wild-type strains. The tec transductant produced long filaments in the absence of tetracaine and had an altered colonial morphology, it reverted at high frequency, with the morphological abnormalities reverting along with the tetracaine resistance. The pmx transductant had an increased sensitivity to levallorphan and to anionic detergents. In contrast, both lev and tec mutants were more resistant to acriflavine than was the wild type or the pmx transductant. The pmx, lev, and tec loci differed in sensitivity to mitomycin C; the lev strain was more resistant, the tec strain was more sensitive, and the pmx strain was much more sensitive than the wild type. There was no difference in sensitivity to several other dyes and detergents, colicins, or T bacteriophage between the transductant and isogenic wild-type strains. Thus, lev, tec, and pmx loci confer more subtle alterations in the permeability barrier than do lipopolysaccharide-deficient mutants previously studied. 相似文献
76.
Lipid and lipopolysaccharide composition of Escherichia coli surface-altered mutants selected for resistance to levallorphan, tetracaine, and polymyxin.
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Certain mutants of Escherichia coli with an altered permeability barrier have an essentially normal lipopolysaccharide, fatty acid, and phospholipid content, with a slight increase in the membrane protein:lipid ratio. The phospholipid metabolism of the lev and tec strains shows an abnormal response to growth in the selective agents levallorphan and tetracaine, respectively. 相似文献
77.
78.
Sellon DC Knowles DP Greiner EC Long MT Hines MT Hochstatter T Hasel KM Ueti M Gillis K Dame JB 《The Journal of parasitology》2004,90(4):782-788
Sarcocystis neurona is an apicomplexan parasite that is the primary etiologic agent of equine protozoal myeloencephalitis in horses. Protective immune responses in horses have not been determined, but interferon-gamma (IFN-gamma) is considered critical for protection from neurologic disease in mice. The role of adaptive and innate immune responses in control of parasites was explored by infecting BALB/c, IFN-gamma knockout (GKO), and severe combined immune deficient (SCID) mice with S. neurona (10(4) sporocysts/mouse). Immune competent BALB/c mice eliminated parasites within 30 days, with no sign of neurologic disease, whereas GKO mice developed fulminant neurologic disease. In contrast, SCID mice remained healthy throughout the experimental period despite the persistence of parasite at low levels in some mice. Treatment with anti-IFN-gamma antibody resulted in neurologic disease in infected SCID mice. Although SCID mice lack adaptive immune responses, they have natural killer (NK) cells capable of producing significant quantities of IFN-gamma. Therefore, SCID mice were infected with sporocysts of S. neurona and treated with anti-asialo GM1. Depletion of NK cells, confirmed by flow cytometry, did not result in neurologic disease in SCID mice. These results indicate that IFN-gamma mediates protection from neurologic disease in SCID mice. Protective levels of IFN-gamma may originate from a low number of nondepleted NK cells or from a non-T cell, non-NK cell population. 相似文献
79.
80.
The carrying capacity of suspension feeding bivalvesin 11 coastal and estuarine ecosystems is examined. Bivalve carrying capacity
is defined in terms of watermass residence time, primary production time andbivalve clearance time. Turnover times for the
11ecosystems are compared both two and threedimensionally. Fast systems, e.g., Sylt and NorthInlet, have turnover times of
days or less, while,slow systems, e.g., Delaware Bay, have turnover timesof months and years. Some systems,Marennes-Oléron,
South San Francisco Bay and NorthInlet, require a net influx of phytoplankton in orderto support their bivalve populations.
Three systems,Carlingford Lough, Chesapeake Bay and Delaware Bay,have very long bivalve clearance times due to small orreduced
bivalve filter feeder populations. Carlingford Lough stands out because it is a naturallyplanktonic system now being converted
to bivalveculture with an adherently stronger benthic-pelagiccoupling.
Existing models of bivalve carrying capacity arereviewed. The Herman model is utilized as anappropriate ecosystem level model
to examine carryingcapacity because it includes the three major turnovertime elements of water mass residence time, primaryproduction
time and bivalve filter feeder clearancetime.
The graphical analysis suggests that massive andsuccessful bivalve filter feeder populations are foundin systems with relatively
short residence times(<40 days) and short primary production times (<4days) in order to sustain a high bivalve biomass withits
associated rapid clearance times. Outliersystems are constrained by long water mass residencetimes, extended primary production
times, and longclearance times.
This revised version was published online in August 2006 with corrections to the Cover Date. 相似文献