Calcium binding to the subunit c ofE. coli ATP-synthase and possible functional implications in energy coupling

The 8-kDa subunit c of theE. coli F₀ ATP-synthase proton channel was tested for Ca⁺⁺ binding activity using a⁴⁵Ca⁺⁺ ligand blot assay after transferring the protein from SDS-PAGE gels onto polyvinyl difluoride membranes. The purified subunit c binds⁴⁵Ca⁺⁺ strongly with Ca⁺⁺ binding properties very similar to those of the 8-kDa CF₀ subunit III of choloroplast thylakoid membranes. The N-terminal f-Met carbonyl group seems necessary for Ca⁺⁺ binding capacity, shown by loss of Ca⁺⁺ binding following removal of the formyl group by mild acid treatment. The dicyclohexylcarbodiimide-reactive Asp-61 is not involved in the Ca⁺⁺ binding, shown by Ca⁺⁺ binding being retained in twoE. coli mutants, Asp61Asn and Asp61Gly. The Ca⁺⁺ binding is pH dependent in both theE. coli and thylakoid 8-kDa proteins, being absent at pH 5.0 and rising to a maximum near pH 9.0. A treatment predicted to increase the Ca⁺⁺ binding affinity to its F₀ binding site (chlorpromazine photoaffinity attachment) caused an inhibition of ATP formation driven by a base-to-acid pH jump in whole cells. Inhibition was not observed when the Ca⁺⁺ chelator EGTA was present with the cells during the chlorpromazine photoaffinity treatment. An apparent Ca⁺⁺ binding constant on the site responsible for the UV plus chlorpromazine effect of near 80–100 nM was obtained using an EGTA-Ca⁺⁺ buffer system to control free Ca⁺⁺ concentration during the UV plus chlorpromazine treatment. The data are consistent with the notion that Ca⁺⁺ bound to the periplasimic side of theE. coli F₀ proton channel can block H⁺ entry into the channel. A similar effect occurs in thylakoid membranes, but the Ca⁺⁺ binding site is on the lumen side of the thylakoid, where Ca⁺⁺ binding can modulate acid-base jump ATP formation. The Ca⁺⁺ binding to the F₀ and CF₀ complexes is consistent with a pH-dependent gating mechanism for control of H⁺ ion flux across the opening of the H⁺ channel.This work was supported in part by grants from the Department of Energy and the U.S. Department of Agriculture.On leave from the Institute of Soil Science and Photosynthesis, Russian Academy of Science, Pushchino, Russia.     

48例原发性闭经患者的细胞遗传学分析

本文报告对48例原发闭经患者的临床和细胞遣传学分析,共发现染色体异常17例,占35.4%,其中包括45,X,7例;45,X/46,XX,2例;X染色体结构异常5例;核型中有Y染色体3例。讨论了原发闭经的细胞遗传学病因及异常核型与表型的关系。     

一个恢复力受单基因控制的水稻CMS育性回复突变体

利用￣（６０）Ｃｏ－γ射线对具有印尼水田谷细胞质的籼稻细胞质雄性不育系Ⅱ－３２Ａ干种子进行诱变处理,获得了一育性回复突变体Ｔ２４。育性基因未纯合的突变体分离出可育株和完全不育株,比例为３∶１;其与Ⅱ－３２Ａ和珍汕９７Ａ测交,Ｆ１代分离出１∶１的可育株和不育株。育性稳定株系与Ⅱ－３２Ａ和珍汕９７Ａ杂交,Ｆ２分离成３∶１的可育株和不育株。表明其育性回复是由一对基因显性突变所致。这一突变体对不育系的育性恢复机制不同于明恢６３、２０９６４等恢复系,后者表现为两对显性恢复基因作用。未观察到Ｔ２４与亲本Ⅱ－３２Ａ除育性以外的其他性状的差异,因而两者构成育性恢复基因的近等基因系。本文还对不育系育性回复类型和Ｔ２４的理论意义与育种价值进行了讨论。     

病毒基因组启动子识别的人工神经网络方法

本文运用神经网络方法,并结合病毒基因分子生物学有关理论与统计事实,对病毒基因启动子区域进行了识别,文中选择了共35个基因组,作为研究对象．学习组选择了28个基因组,预测组选择了7个基因组,结果表明,将神经网络模型与病毒基因有关理论相结合,能够运用计算方法,以大量的可能启动子组合中排列出唯一的启动子区域．     

多年生黑麦草草地生态系统中放牧强度对草地结构及组织转化的影响

研究了放牧强度对多年生黑麦草人工草地蘖的形态、密度、草地生产率及组织转化的影响。结果表明,重牧条件下蘖密度大于轻牧,而轻牧的单株蘖重大于重牧。重牧划地净生产率大于轻牧,主要是由于轻和手条件下,草地的高的生长率被更高的枯死率所抵消。春夏之交,采用灵活的管理措施,转换放牧强度可以提高草地的生产率。     

中国无患子科的地理分布

无患子科是一个乏热带分布科,全世界有１４４属,１６８０种,本文着重阐述：１．无患子科的分类系统及演化;２．世界无患子科的地理分布;３．中国无患子科的地理分布;４．无患子科的早期化地点及散布途径。结果表明无患子科现代分布变异中心在亚洲（印度－马西亚）－非洲－南美洲。中国无患子科有２５属,５４种,特有成分外,均与印度一马来西亚共有,大多数位于分布区的边缘。根据化石记录及现代及分布推断,无患子科可能在白     

生态蛇胆美容霜对治疗蠕形螨病及护肤美容的效果观察

本文报道了微生态制剂－生态蛇胆美容霜治疗蠕形螨病及其合并症的观察结果。用透明胶带定量计数法检查１１３１人,其中检出毛囊虫阳性者４０４例,定居率为３５．７％,检出毛囊出共４１８只。对４０４例毛囊虫阳性分两组,即实验组,和对照组进行对照。结果实验组２５１例中只有２例仍为阳性,其余转为阴性。     

湿地松粉蚧夏季数量凋落的原因分析

利用生命表技术及其相应的控制指数分析方法,对新侵入害虫湿地松粉蚧Ｏｒａｏｅｌｌａａ－ｃｕｔａ（Ｌｏｂｄｅｌｌ）夏季数量凋落的某些因子进行了量化分析。结果表明：在广东南部的新侵入区,夏季高温引起的松梢迅速老化,上代为害以后引起的营养质量的变化、拥挤以及煤污病的严重发生等,均对湿地松粉蚧夏季种群数量的凋落有着明显的影响,其总的排除作用控制指数ＥＩＰＣ为４６．８９,如果排除这几个因子的作用,下代种群的数量将为当代的４６．８９倍。     

L-异亮氨酸和甘氨酸对大肠杆菌表达与分泌邻苯二酚2,3-双加氧酶的作用

证实了甘氨酸与L-异亮氨酸对大肠杆菌表达邻苯二酚2,3-双加氧酶(CatO_2ase)的促进作用和甘氨酸促使该酶分泌至胞外培养基中的作用.产酶量高低和分泌量多少与培养基种类、甘氨酸和L-异亮氨酸的浓度以及培养时间等因素有关.在甘氨酸存在的情况下,胞壁对溶菌酶的敏感性有所增加,超微形态似有变化,还存在其他物质的伴随分泌,故甘氨酸可能是引起细胞壁结构的改变而导致邻苯二酚2,3-双加氧酶等胞内容物被动分泌至胞外.     

Flow-induced detachment of red blood cells adhering to surfaces by specific antigen-antibody bonds.

Fixed spherical swollen human red blood cells of blood type B adhering on a glass surface through antigen-antibody bonds to monoclonal mouse antihuman IgM, adsorbed or covalently linked on the surface, were detached by known hydrodynamic forces created in an impinging jet. The dynamic process of detachment of the specifically bound cells was recorded and analyzed. The fraction of adherent cells remaining on the surface decreased with increasing hydrodynamic force. For an IgM coverage of 0.26%, a tangential force on the order of 100 pN was able to detach almost all of the cells from the surface within 20 min. After a given time of exposure to hydrodynamic force, the fraction of adherent cells remaining increased with time, reflecting an increase in adhesion strength. The characteristic time for effective aging was approximately 4 h. Results from experiments in which the adsorbed antibody molecules were immobilized through covalent coupling and from evanescent wave light scattering of adherent cells, imply that deformation of red cells at the contact area was the principal cause for aging, rather than local clustering of the antibody through surface diffusion. Experiments with latex beads specifically bound to red blood cells suggest that, instead of breaking the antigen-antibody bonds, antigen molecules were extracted from the cell membrane during detachment.