Stem cells, cancer, and cancer stem cells.

Stem cell biology has come of age. Unequivocal proof that stem cells exist in the haematopoietic system has given way to the prospective isolation of several tissue-specific stem and progenitor cells, the initial delineation of their properties and expressed genetic programmes, and the beginnings of their utility in regenerative medicine. Perhaps the most important and useful property of stem cells is that of self-renewal. Through this property, striking parallels can be found between stem cells and cancer cells: tumours may often originate from the transformation of normal stem cells, similar signalling pathways may regulate self-renewal in stem cells and cancer cells, and cancer cells may include 'cancer stem cells' - rare cells with indefinite potential for self-renewal that drive tumorigenesis.     

甲（乙）基在甲（乙）苯亲电取代反应中的定位作用和定位能力讨论

在有机化学的亲电取代反应定位法则教学中,甲基代表烷基,作为芳烃亲电取代反应定位效应的典型例子,但甲基不同于乙基等烷基,具有不同的定位能力,烷基是如何影响芳环的结构从而影响取代基定位,教材和教学中描述较简单,不便于学生领会和比较。该文就此问题进行探讨,结果表明,烷基苯RAr（R—Me、Et）的R在空间的位置影响烷基苯的能量和原子电荷密度,从而影响烷苯的亲电取代反应。（1）烷苯的R—Ar键旋转形成不同构象,其中的最大与最小体系能量值之差△E,△E（Me）〈△E（Et）,{△E（Me）=0．0000084a．u,△E（Et）=0．0068029a．u},甲苯比乙苯的R—Ar单键更容易自由旋转。在EtAr,C8-C7-C1平面与苯环垂直时,体系能量[E（90）=-308．661166a．u．]最低,为较稳定的优势构象。（2）甲基和乙基均向苯环供电子,虽甲（乙）苯环的碳原子所带电荷之和都不及苯,但甲苯比乙苯的环碳上电子密度大,∑Q（Me,30）=-1．02794〈∑Q（Et,90）=-1．010487。（3）甲（乙）苯化合物中,均为邻、对位碳原子电子密度大于苯环碳{甲基：邻位qc2（30）=qc6（30）=-0．212118,对位-0．20724～-0．20728;乙基：邻位qc2（90）=qc6（90）=-0．209509,对位q（90）（-0．20695）},间位碳原子的电子密度小于苯环碳[甲基间位-0．19153～-0．19228;乙基间位q（90）=-0．192171],甲、乙苯的邻、对位有利于亲电取代反应,且甲基大于乙基的定位能力。（4）亲电试剂Me^＋与苯环反应形成邻、对位的碳正离子中间体比闯位碳正离子中间体稳定,有利于生成邻、对位取代产物,因此,甲、乙基均为邻、对位定位基。     

Coordination of circadian timing in mammals

Time in the biological sense is measured by cycles that range from milliseconds to years. Circadian rhythms, which measure time on a scale of 24 h, are generated by one of the most ubiquitous and well-studied timing systems. At the core of this timing mechanism is an intricate molecular mechanism that ticks away in many different tissues throughout the body. However, these independent rhythms are tamed by a master clock in the brain, which coordinates tissue-specific rhythms according to light input it receives from the outside world.     

多出/入口仓库的货位优化研究

在“人到货”多出/入口仓库货位优化问题中,为了减少库内整体作业时间,提高拣选效率,基于多维标度分析算法(dimensional scaling analysis algorithm, MDS)与峰值聚类算法(peak clustering algorithm, DPC),提出以货品相关性为基础的货位优化方法。首先通过历史订单数据进行分析获得货品相关度矩阵,并利用多维标度分析算法对相关度矩阵进行数据处理,在仓库实际情况下确定合适数量聚类簇后,采用峰值聚类算法将相关性高的货品聚类形成一个具有高相关性货品集合,再据货品集合优化存储区域。最后,通过实际案例进行分析,比较本文存储策略与原始存储策略在跨区域拣选条件下订单平均拣选距离,并通过本文优化策略与随机策略在相同规模订单情况下比较验证,结果显示,本文策略比随机策略优化平均优化24.56%,有效地提高了订单拣选效率。     

钢筋受压黏结滑移模型

为研究钢筋的受压黏结滑移关系,采用分辨率较高的激光位移计,对一批短锚长试件进行系列推出试验研究,得到精确度较高的黏结滑移值及完整的试验黏结滑移关系曲线,描述钢筋在混凝土中的受压黏结滑移破坏全过程:弹性阶段、局部滑移阶段、滑移上升段、滑移下降段和残余段.在对试验得到的较短锚长试件推出试验结果分析的基础上,经统计回归和分析,提出钢筋的受压黏结滑移曲线模型,并与试验结果进行对比.     

Male development of chromosomally female mice transgenic for Sry

The initiation of male development in mammals requires one or more genes on the Y chromosome. A recently isolated gene, termed SRY in humans and Sry in mouse, has many of the genetic and biological properties expected of a Y-located testis-determining gene. It is now shown that Sry on a 14-kilobase genomic DNA fragment is sufficient to induce testis differentiation and subsequent male development when introduced into chromosomally female mouse embryos.     

Membrane protein oligomeric structure and transport function

Proteins which traverse membranes tend to have a dimeric structure in which the dimer is arranged asymmetrically across the membrane with the axis of symmetry perpendicular to the membrane plane. This general structure is well suited to the function of transporting nutrients across the cell membrane.     

Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease.

A locus segregating with familial Alzheimer's disease (AD) has been mapped to chromosome 21, close to the amyloid precursor protein (APP) gene. Recombinants between the APP gene and the AD locus have been reported which seemed to exclude it as the site of the mutation causing familial AD. But recent genetic analysis of a large number of AD families has demonstrated that the disease is heterogeneous. Families with late-onset AD do not show linkage to chromosome 21 markers. Some families with early-onset AD show linkage to chromosome 21 markers, but some do not. This has led to the suggestion that there is non-allelic genetic heterogeneity even within early onset familial AD. To avoid the problems that heterogeneity poses for genetic analysis, we have examined the cosegregation of AD and markers along the long arm of chromosome 21 in a single family with AD confirmed by autopsy. Here we demonstrate that in this kindred, which shows linkage to chromosome 21 markers, there is a point mutation in the APP gene. This mutation causes an amino-acid substitution (Val----Ile) close to the carboxy terminus of the beta-amyloid peptide. Screening other cases of familial AD revealed a second unrelated family in which this variant occurs. This suggests that some cases of AD could be caused by mutations in the APP gene.