Thick and thin fingers point out Turing waves

Mouse genetics and computer simulations demonstrate that digit number and width are controlled by a Turing-type mechanism in which distal Hox genes modulate periodicity.     

甲亢甲低患者肝纤维化指标检测的临床意义分析

目的:探讨甲状腺功能亢进(甲亢)、甲状腺功能减低(甲低)与肝纤维化指标的关系及其可能的机制。方法:采用放射免疫分析法(R1A)检测57例甲亢患者、43例甲低患者、39例甲亢治疗后甲状腺激素正常者和50例健康成人的血清Ⅳ型胶原(1V-C)、Ⅲ型前胶原(PCⅢ)、透明质酸(HA)、层粘连蛋白(LN)、T3、T4、FT3、FT4、TSH、TGA、TMA含量。结果:甲亢患者组血清中1V-C、PCⅢ含量比正常对照组及甲低患者组显著性增高(P<0.05);治疗后甲状腺激素下降,1V-C、PCⅢ含量也随之下降(与治疗前比较P<0.01);HA、LN在四组中无显著性差异(P>0.05),在甲亢治疗前后无显著性差异(P>0.05)。各项肝纤维化指标与TGA、TMA的阳性率无关。结论:甲亢患者可有不同程度的肝功能损害,血清中甲状腺激素水平增高时,1V-C、PCⅢ水平也增高,在用1V-C、PCⅢ判断肝纤维化时应注意有无甲状腺疾病特别是甲亢。未发现HA、LN含量与甲状腺激素水平的关系。     

塔里木盆地西北缘核桃坚果生化成分多样性分析

该研究收集新疆塔里木盆地西北缘44份核桃资源,其中树龄超过50 a的实生资源41份、主栽良种3个,并对其主要生化成分蛋白质、糖、脂肪、氨基酸、油酸、亚油酸、亚麻酸、棕榈酸、硬脂酸进行了多样性分析。结果表明:44份资源的生化成分变异幅度大,存在着丰富的多样性。各指标变异幅度由4.93%~30.93%,香农-维纳指数(H')变幅为1.38~2.02。17种氨基酸变异幅度由10.07%~35.71%,香农-维纳指数(H')变幅为1.85~2.20。主要生化成分主成分分析显示蛋白质、糖、脂肪三个主要成分的累计贡献率达81.67%。聚类分析表明,群组间生化成分存在显著差异,群组的聚类与地理分布有明显相关性,流域相同的资源的生化成分构成比例具有相似性。与主栽品种相比,实生资源在糖、蛋白质、脂肪等方面具有更高的变异幅度,因而具有一定的开发潜力。     

单细胞测序方法研究进展

近年来,高通量测序技术(Next-generation sequencing,NGS)快速发展,已广泛应用于生命科学各个领域,但传统的混合细胞测序(Bulk cell sequencing)检测的是细胞群体的总平均反应,无法反应每个细胞的真实情况,这会影响研究者对细胞功能认知的准确性。单细胞测序技术(Single cell sequencing,sc-Seq)的出现,从一定程度上解决了传统测序固有的缺陷。单细胞测序是针对单个细胞的RNA或DNA进行测序,能够准确测出单个细胞的基因结构和表达状态,从而分析相同表型细胞的异质性。本文首先介绍单细胞测序的原理、测序类型和测序平台,有助于理解单细胞测序和在进行科研项目时设计合适的项目方案。进一步介绍单细胞转录组测序的分析流程和各种常用的分析工具或软件,并重点阐述单细胞转录组测序分析中的细胞聚类和拟时序分析的原理和研究进展,为进行单细胞转录组测序数据分析提供参考。最后,本文简述了单细胞测序研究热度、单细胞测序的应用、挑战和展望等,有助于更全面地认识单细胞测序。     

关联维数法在皮肤激光散斑测量中的应用

本文采用关联维数方法研究了皮肤厚度对皮肤激光散斑测量的影响。计算了６种模拟皮肤厚度情况下的生物散斑关联维数。结果表明,维数随皮肤厚度的增加而减小,而且重复性很好。这说明,关联维数方法可以应用在皮肤激光散斑的研究中     

脂肪间充质干细胞来源外泌体的功能

外泌体是细胞外膜质纳米囊泡,将蛋白质、核酸(DNA和RNA)转运到靶细胞中,介导局部和系统的细胞间通信,从而改变受体细胞的行为.这些小泡在许多生物功能中发挥重要作用,如脂肪合成、免疫调节、神经再生和肿瘤调节等.脂肪间充质干细胞目前被认为是细胞治疗和再生医学领域中一种功能丰富的工具,可产生和分泌多种外泌体,继承细胞的多种...     

Abnormal Epidermal Keratinization in the repeated epilation mutant mouse

Repeated epilation (Er) is a radiation-induced, autosomal, incomplete dominant mutation in mice which is expressed in heterozygotes but is lethal in the homozygous condition. Many effects of the mutation occur in skin: the epidermis in Er/Er mice is adhesive (oral and nasal orifices fuse, limbs adhere to the body wall), hyperplastic, and fails to undergo terminal differentiation. Skin from fetal +/+, Er/+ and Er/Er mice at ages pre- and postkeratinization examined by light, scanning, and transmission electron microscopy showed marked abnormalities in tissue architecture, differentiation, and cell structure; light and dark basal epidermal cells were separated by wide intercellular spaces, joined by few desmosomes, and contained phagolysomes. The numbers of spinous, granular, and superficial layers were highly variable within any given region and among various regions of the body. In some areas, 2-8 layers of granular cells, containing large or diminutive keratohyalin granules, extended to the epidermal surface; in others, the granular layers were covered by several layers of partially keratinized or nonkeratinized cells. In rare instances, a single or small group of cornified cells was present among the granular layers but was not associated with the epidermal surface. Both the granular and nonkeratinized/partially keratinized upper epidermal layers Er/Er skin gave positive immunofluorescence with antiserum to the histidine-rich, basic protein, filaggrin. Proteins in epidermal extracts from +/+, Er/+ and Er/Er mice were separated and identified by radio- and immunolabeling techniques. The Er/Er extract was missing a 26.5- kdalton protein and had an altered ratio of bands in the keratin region. The 26.5-kdalton band was histidine-rich and cross-reacted with the antiserum to rat filaggrin. Several high molecular weight bands present in both Er/Er and +/+ extracts also reacted with the antiserum. These are presumed to be the precursors of filaggrin and to account for the immunofluorescence om Er/Er epidermis even though the product protein is absent. The morphologic and biochemical data indicated that the genetic defect has a general and profound influence on epidermal differentiation, including alteration of two proteins (filaggrin and keratin) important in normal terminal differentiation, tissue architecture, and cytology. Identification of epidermal abnormalities at early stages of development (prekeratinization) and defective structure of other tissues and gross anatomy suggest that the mutation is responsible for a defect in same regulatory step important in many processes of differentiation and development.     

Isolation and characterization of the major form of polyprenyl-phospho- mannose from Mycobacterium smegmatis

We isolated from the endogenous polyprenyl-phospho-sugar pool of Mycobacterium smegmatis two mannose-containing compounds, i.e., a partially saturated C35-octahydroheptaprenyl-P-mannose and a fully unsaturated C50-decaprenyl-P-mannose. The relative amount of C35- polyprenyl-P-mannose in mycobacterial cells was comparable to that of decaprenyl- P-pentoses and, at least, an order of magnitude higher than that of C50-decaprenyl-P-mannose. The major form of mycobacterial polyprenyl-P-mannose was structurally characterized by combined gas chromatography-mass spectrometry, fast-atom bombardment tandem mass spectrometry and proton-nuclear magnetic resonance spectroscopy as beta- d-mannopyranosyl-monophospho-(C35)octahydroheptapren ol of which all three isoprene units have Z ( cis ) configuration. The differences in the structure and cellular concentrations of the mycobacterial mannosyl- P-polyprenols reflect distinct biochemical pathways of the two compounds and suggest the existence of specific GDP-Man:polyprenyl-P mannosyltransferases (synthetases) able to distinguish between C35- octahydroheptaprenyl- and C50-decaprenyl- phosphates of mycobacteria. Since the 6'-O-mycoloylated form of C35-octahydroheptaprenyl-P-mannose isolated from M. smegmatis is apparently involved in mycolate rather than mannosyl transfer reactions, we speculate that a catabolic pathway responsible for degradation of C35-P-mannose and recycling C35- octahydroheptaprenyl phosphate might exist in mycobacteria.      

犬MC1R基因R306ter与毛色性状相关性研究

目的　分析犬MC1R基因中R30 6ter位点多态性与犬毛色表型的相关性 ,为遗传育种 ,培育出更加优良的实验用犬奠定基础。方法　采用PCR SSCP技术 ,对MC1R基因R30 6ter位点进行基因多态性检测 ,分析位点多态性与毛色性状之间的相关性 ,并对该位点进行克隆测序。结果　PCR SSCP分析结果表明 ,R30 6ter位点序列具有多态性 ,表现为C、D二个等位基因和CC、CD及DD三种基因型。对R30 6ter多态性片段克隆测序发现 ,MC1R基因在编码第 30 6位氨基酸的密码子处存在一个由CGA到TGA的终止突变。结论　经统计分析结果表明在杂种犬中MC1R基因多态性与毛色性状不存在显著的相关性 ,这可能是由于外科手术学教学用犬是杂种犬 ,其遗传背景不同所致。由于MC1R基因的R30 6ter位点内存在碱基变异 ,因此在杂种犬中表现出明显的PCR SSCP多态性