钼,铁,硫化合物激活曝氧的棕色固氮菌固氮酶钼铁蛋白的研究

曝氧后,棕色固氮菌(Azotobacter vinelandii)固氮酶钼铁蛋白的催化活性和圆二色信号都显著降低,而吸收光谱则显著增加。与钼、铁、硫化合物和二硫苏糖醇组成的重组溶液保温后,曝氢蛋白的圆二色信号和吸收光谱几乎完全恢复至天然状态的同时,乙炔还原活性也得到了显著的恢复,表明重组溶液可使曝氧蛋白中的 P-cluster和其它活性部位都得到了不同程度的修复。     

记内蒙古Juxia一新种

本文记述了在内蒙古沙拉木伦额尔登敖包地区第三系下渐新统乌兰戈楚组中发现的始巨犀的一个新种:寿氏始巨犀(Juxia shoui)。据其前臼齿及鼻切迹的位置等特点,这一新种当为始巨犀属中比较进步的一个成员,是包氏始巨犀和巨犀之间的过渡类型的犀类动物。     

兴安落叶松结实规律与长短枝习性的关系

1987年5月,大兴安岭林区发生的特大森林火灾,实属世界罕见,火灾面积达1.0×10~6ha 多。大量的火烧迹地亟待更新、无论是人工更新还是人工促进天然更新,其中关键的问题之一是种子的来源,在大兴安岭地区,兴     

红松越冬针叶的电子自旋共振（ESR）波谱

用ESR波谱仪在越冬红松针叶及叶绿体冻干粉中检出了g值分别为2.0044和2.0037的明确的单峰信号。针叶伤害愈重,信号愈强。此信号可被Vc或富含SOD等多种自由基清除剂的沙棘果汁所抑制。针叶受害愈重,沙棘果汁对信号的抑制作用愈强,Vc的抑制作用愈弱。据此认为红松苗越冬伤害和有机自由基的形成有关。在伤害发展的不同阶段,有机自由基的种类组成也不同。     

禄丰古猿化石地点的植物叶化石

1987年,在云南禄丰古猿化石地点D剖面第4层(薄层黑色炭质粘土与灰色细砂互层)发现植物叶部印痕化石,经鉴定属壳斗科绝灭的雷龙潭槲叶(Dryophyllum relongtanense Colani),该种植物常参与组成亚热带至暖温带的常绿阔叶林或常绿与落叶阔叶混交林。     

环状病毒M14 dSRNA基因组的进一步研究

M14病毒是1981年从北京郊区捕获的三带喙库蚊中分离获得。其生物学、形态学和理化特性均符合呼肠孤病毒科环状病毒的特点。聚丙烯酰胺凝胶电泳将其dsRNA基因组分离成11条区带。但最近的进一步研究发现,它是由12个片段的RNA组成。又用猴轮状病毒SA11株作为标准,测定了每个片段的分子量。 白纹伊蚊细胞C6/36纯系,由日本长畸大学热带医学研究A.Igarashi教授惠赠,并照他的方法培养传代。     

固氮酶铁钼辅因子FeMo-co在水与非水体系内重组活力与催化活力的比较研究

 本文提出一种测定FeMo-co催化活力的反应体系,用此反应体系,在测定FeMo-co催化活力的过程中,FeMo-co与变种UW45抽提液的重组活性始终保持不变。讨论了水含量、还原剂对FeMo-co催化活力和重组活力的影响。     

不同底物与固氮酶及其钼铁蛋白相互作用的荧光光谱分析

 本文研究了不同底物(N_2,H_2,N_2O,NaN_3,C_2H_2)对棕色固氮菌固氮酶及其钼铁蛋白荧光光谱的影响。结果表明,上述底物均能络合在钼铁蛋白及固氮酶上,但络合程度不同,从而为固氮酶系统有多个不同的底物络合中心,底物络合中心在钼铁蛋白分子上,铁蛋白对钼铁蛋白有变构作用,提供了光谱学证据。     

Ethanol Inhibits Basic Fibroblast Growth Factor-Mediated Proliferation of C6 Astrocytoma Cells

Abstract: Early ethanol exposure alters the proliferative activity of glial and neuronal precursors in the developing CNS. The present study tests the hypothesis that ethanol-induced alterations in cell proliferation result from interference with growth factors. An in vitro model of astroglia (C6 astrocytoma cells) was used to study the effects of ethanol on proliferation mediated by basic fibroblast growth factor (bFGF). bFGF stimulated the proliferation of C6 cells. This bFGF-enhanced proliferation was evident by increases in total cell number, DNA synthesis (as measured by [³H]thymidine incorporation), and the number of cells that took up bromodeoxyuridine. A synthetic peptide that specifically blocked the binding of bFGF to its high-affinity receptor completely abolished the proliferation-promoting effect of bFGF. The action of another mitogen for C6 cells, insulin-like growth factor-1, was not affected by this peptide. Therefore, the bFGF-stimulated proliferation was mediated through a specific bFGF receptor. Ethanol inhibited bFGF-mediated proliferation in a concentration-dependent manner. Ethanol concentrations of 100 and 200 mg/dl partially inhibited bFGF-mediated proliferation (by 58 and 74%, respectively), whereas concentrations of ≥400 mg/dl completely abolished the growth-stimulating effect of bFGF. Our data show that ethanol alters proliferative activity of C6 cells by disrupting the action of bFGF. The target of ethanol neurotoxicity is a receptor-mediated activity. bFGF can affect cell proliferation by a non-receptor-mediated intracellular pathway, but ethanol does not have an impact on this pathway.