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991.
L7811鼠腹水肿瘤细胞^31P核磁共振的研究 总被引:1,自引:0,他引:1
用~(31)P核磁共振技术(~(31)P-NMR)研究了L_(7811)鼠腹水肿瘤细胞和615系鼠胸腺细胞(正常对照细胞)。结果发现在肿瘤晚期阶段,L_(7811)腹水肿瘤细胞的含磷化合物未进入完全不活跃状态。此外,腹水肿瘤细胞的磷脂组成与含量亦有明显改变。因此,~(31)P-NMR谱可做为观察肿瘤细胞内能量生成和某些磷脂合成宏观动态过程的一项参考指标。 相似文献
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996.
自病人气管灌洗物中分离出一株嗜肺性军团杆菌 总被引:1,自引:0,他引:1
本文报道了用自制的蓝藻军团杆菌选择性培养基从病人气管灌洗物中分离到一株嗜肺性军团杆菌(Legionella pneumophila)并与BCYE及硝酸铁琼脂平板等培养基作了比较,发现该菌在蓝藻军团杆菌选择性培养基上生长最好。生化、动物试验;细菌学、血清学的鉴定和诊断及临床治疗效果观察均与军团病杆菌(LDB)的鉴定标准相符合,证明经分离得的是一株嗜肺性军团杆菌血清6型菌株。 相似文献
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998.
Shlomo Nir Nejat Düzgünes Maria C. Pedroso De Lima Dick Hoekstra 《Cell biochemistry and biophysics》1990,17(2):181-201
The fusion of viruses with cells and liposomes is reviewed with focus on the analysis of the final extents and kinetics of
fusion.Influenza virus andSendai virus exhibit 100% of fusion capacity with cells at pH 5 and pH 7.5, respectively. On the other hand, there may be in certain
cases, a limit on the number of virions that can fuse with a single cell, that is significantly below the limit on binding.
It still remains to be resolved whether this limit reflects a limited number of possible fusion sites, or a saturation limit
on the amount of viral glycoproteins that can be incorporated in the cellular membrane, like the case of virus fusion with
pure phospholipid vesicles, in which the fusion products were shown to consist of a single virus and several liposomes. Both
viruses demonstrate incomplete fusion activity towards liposomes of a variety of compositions. In the case ofSendai virus, fusion inactive virions bind essentially irreversibly to liposomes. Yet, preliminary results revealed that such bound,
unfused virions can be released by sucrose gradient centrifugation. The separated unfused virions subsequently fuse when incubated
with a “fresh” batch of liposomes. We conclude, therefore, that the fraction of initially bound unfused virions does not consist
of dective particles, but rather of particles bound to liposomes via “inactive” sites.
Details of the low pH inactivation of fusion capacity ofinfluenza virus towards cells and liposomes are presented. This inactivation is caused by protonation and exposure of the hydrophobic
segment of HA2, and affects primarily the fusion rate constants. Some degree of inactivation also occurs when virions are bound to cellular
membranes. 相似文献
999.
The inhibitory effects of synthetic phenolic compounds on benzo(a)pyrene-induced neoplasia of the mouse forestomach have been measured by Wattenberg et al6 The efficiency of this inhibition has been estimated for each phenol, using R, the ratio of the number of tumors per mouse in the protected group over the number of tumours per mouse in the control group. We have observed a linear correlation between the chemoprotection efficiency R and the logarithm of the rate of quenching of singlet oxygen. k. by this family of phenols, log k being itself correlated with the one-electron oxidation potential of the phenols. These correlations suggest a charge transfer mechanism for the inhibition of neoplasia induced hy benzo(a)py-rene. The correlations described provide a theoretical basis for scaling the inhibitors of mutagenicity induced by polycyclic aromatic compounds in terms of their oxidation potentials 相似文献
1000.
Quinones may be toxic by a number of mechanisms. including arylation and oxidative stress caused by redox cycling. Using isolated hepatocytes, we have studied the cytotoxicity of four quinones. with differing abilities to arylate cellular nucleophiles and redox cycle. in relation to their effects on cellular pyridine nucleotides. High concentrations of menadione (redox cycles and arylates). 2-hydroxy-1,4-naphthoquinone (neither arylates nor redox cycles via a one electron reduction) 2.3-dimethoxy-1.4-naphthoquinone (a pure redox cycler) and p-benzoquinone (a pure arylator) caused an initial decrease in NAD+ and loss of viability, which was not prevented by 3-aminobenzamide. an inhibitor of poly(ADP-ribose)polymerase. In contrast. 3-aminobenzamide inhibited the loss of NAD' and viability caused by dimethyl sulphate so implicating poly(ADP-ribose)polymerase in its toxicity but not that of the quinones. Non-toxic concentrations of menadione. 2.3-dimethoxy-1.4-naphthoquinone and 2-hydroxy-1.4-naphthoquinone all caused markedly similar changes in cellular pyridine nucleotides. An initial decrease in NAD+ was accompanied by a small. transient increase in NADP+ and followed by a larger. prolonged increase in NADPH and total NADP+ + NADPH. Nucleotide changes were not observed with non-toxic concentrations of p-benzoquinone. Our findings suggest that a primary event in the response of the cell to redox cycling quinones is to bring about an interconversion of pyridine nucleotides. in an attempt to combat the effects of oxidative stress 相似文献