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91.
以稀释倒平板法从0型菌086和IV型菌967-4和9620中分离到59个单细胞系;在12个近等基因系品种上,086和其单细胞系表现为弱毒力,2个IV型菌及其单细胞系能克服抗病基因Xa-1、2、3、8、10、11、14的抗性,不能克服Xa-21、4、5、7、13的抗性;带主效抗病基因的品种Asominori、XM5、M41、XM6和丰锦能把3个母株的59个单细胞系区分为12种数量差异或质量差异的不同致病型;将此5品种与近等基因系配合,适合作为病菌致病基因变异频度监测的寄主;采用"段叶沙培,切口取菌胶"法分离病菌,在中国致病型鉴定品种上划分的致病型,是田间病菌群体毒力结构的表型反应。 相似文献
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AIM:To investigate the effect of metallothionein(MT) on proliferation of rat vascular smooth muscle cells (VSMCs) stimulated by homocysteine and its mechanism. METHODS:VSMCs proliferation was measured by [3-H]-TdR incorporation, mitogen-activated protein kinase(MAPK)activity were determined by immunoprecipitation method, the intracellular contents of MT and malondialdehyde (MDA)were assayed by -hemoglobin saturation method and TBA reaction, respectively, and lactate dehydrogenase (LDH) leakage was measured by NADH oxidation. RESULTS:Hcy(10-6-10-4 mmol/L) stimulated [3-H]-TdR incorporation by the VSMCs in a concentration-dependent manner. Compared with control, [3-H]-TdR incorporation in VSMCs treated with 0.1 mmol/L Hcy was increased by 4.2 fold (P<0.01). Meanwhile, Hcy enhanced MAPK activity, MDA formation and LDH release (P<0.01)in a concentration-dependent manner. Treatment of VSMCs with MT alone did not change above parameters, compared with control. However, MT (10-6-10-4 mol/L)attenuated significantly Hcy-stimulated proliferation of VSMCs (P<0.01)in a concentration-dependent manner. And MT inhibited obviously Hcy-induced activation of MAPK activity, MDA formation and LDH release. Preincubation of VSMCs with 0.5 mmol/L ZnCl2 for 6 h induced an increase cellular MT content by 5.7-fold (P<0.01). The MT-overexpressed VSMCs resisted Hcy-stimulating action on MAPK activity, MDA formation and LDH leakage (P<0.01). CONCLUSION:These results show that MT has an inhibitory effect on Hcy-induced VSMCs proliferation, and that MT could inhibit Hcy-stimulated MAPK activity and lipid peroxidation. 相似文献
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AIM:To examine the effects of recombinant human hepatocyte growth factor(rhHGF) and native calf HGF(cHGF) on SMMC-7721 human hepatocellular carcinoma(HCC) cell line. METHODS:Human HCC cell line culture, photometric assay, and flow cytometric assay were used in this study .RESULTS:A similar type of dose-dependent cell growth inhibition effect on SMMC-7721 human HCC cells by rhHGF(5-20 μg/L) as well as by cHGF(25-100 mg/L) had been found, with the maximal effect at the highest concentration used. Approximately over 50% of the cells treated with rhHGF(5 μg/L, 10 μg/L, 20 μg/L) accumulated in the quiescent G0/G1 phase of the cell cycle over incubation periods for 3 d. CONCLUSION:The growth of SMMC-7721 human HCC cells was strongly inhibited by both rhHGF and cHGF. This might be because the cells exposed to HGF became arrested in the G0/G1 phase. 相似文献
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AIM:To study the effect of environment of liver regeneration on the proliferation of rat fetal hepatocytes after intrasplenical transplantation. METHODS:Fetal hepatocytes isolated from 3-week SD rat fetuses bred were transplanted into the spleens of liver regeneration model rats with 70% partial hepatectomy. The cell cycle of the hepatocytes in the remnants liver was analyzed by flow cytometer and the density dimensions of the donor fetal hepatocytes in spleen were measured by image analysis system 7 and 30 days post-transplantation, respectively. RESULTS:Compared with the control group, the proportions of S and G2 /M cells in the remnants liver were obviously decreased (P<0.05), but the density dimensions of the donor fetal hepatocytes in spleen increased significantly (P<0.05) in rats with hepatectomy 7 days post-transplantation. CONCLUSION:The environment of liver regeneration is propitious to the proliferation of fetal hepatocytes after transplantation into spleen. 相似文献
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The major role of DNA polymerase β was thought to be limited in its involvement in short patch base excision repair by removing 5’-deoxyribose phosphate and base insertion. However, the recent researches indicate that polymerase β might take part in a wide spectrum of DNA metabolism reactions, including long patch base excision repair, DNA replication, recombination, meiosis and transleisional DNA synthesis. Because of its wide and important cellular function, an inappropriate intracellular polymerase β level might be associated with genomic instability. Down-regulation or mutation of polymerase β is mutagenic due to deficient in DNA repair, while overexpression of this error-prone β polymerase might perturb the normal function of other accurate polymerases and cause genomic instability as well. 相似文献