广西扶绥岩亮洞早更新世独角犀年龄结构的分析

岩亮洞是广西扶绥地区最近新发现的早更新世巨猿化石点,经过初步发掘,采集到了丰富的巨猿材料及大量伴生的哺乳动物化石。引人注目的是其中犀类化石居多,包括146颗完整的牙齿及十多件头后骨骼化石,从形态特征判断,这些犀类化石应属于独角犀的一新种Rhinoceros fusuiensis。岩亮洞巨猿动物群中的独角犀以种群丰度最大而不同于其他已知东亚地区的巨猿动物群中的独角犀类材料。本文从犀类牙齿的主尖釉质层、齿质暴露程度、咀嚼面的磨蚀程度等方面对岩亮洞独角犀的年龄结构进行了研究。该死亡群中至少有4头幼年个体、5头青年个体、5头成年个体和1头老年个体。依据牙齿磨蚀程度和牙齿萌出顺序对年龄结构的分析及统计显示,其中青年个体和成年个体最多,幼年个体次之,老年个体最少,其死亡的原因不是通常意义上磨耗型死亡,突发性的灾害可能是造成这种死亡年龄分布的主要原因。     

浙江省桐庐县长叶榧居群遗传结构的ISSR分析

采用ISSR分子标记技术,对浙江省桐庐县白云源森林公园的6个长叶榧（Torreya jackii）亚居群进行分析,阐明长叶榧在小地理范围内的遗传结构。12个引物对6个长叶榧亚居群的120个个体进行扩增,共得到194个位点,其中多态位点87个,总多态位点百分率（P）为44.85%,平均为29.21%。长叶榧总Shannon信息指数（I）为0.166 3,平均为0.119 9;总Nei指数（h）为0.103 5,平均为0.075 5。P、I、h均表明长叶榧总体水平的遗传多样性较高,亚居群水平的遗传多样性较低。AMOVA分子变异分析显示,21.45%的变异存在于亚居群间,78.55%的变异存在于亚居群内。长叶榧亚居群间的遗传分化系数（G_st）为0.270 5,基因流为1.347 8。6个长叶榧亚居群的平均遗传距离为0.037 0,根据亚居群间的遗传距离进行UPGMA聚类,结果为生境相似的亚居群聚在一起。     

GSK-3 Phosphorylates ��-Catenin and Negatively Regulates Its Stability via Ubiquitination/Proteosome-mediated Proteolysis

δ-Catenin was first identified because of its interaction with presenilin-1, and its aberrant expression has been reported in various human tumors and in patients with Cri-du-Chat syndrome, a form of mental retardation. However, the mechanism whereby δ-catenin is regulated in cells has not been fully elucidated. We investigated the possibility that glycogen-synthase kinase-3 (GSK-3) phosphorylates δ-catenin and thus affects its stability. Initially, we found that the level of δ-catenin was greater and the half-life of δ-catenin was longer in GSK-3β^−/− fibroblasts than those in GSK-3β^+/+ fibroblasts. Furthermore, four different approaches designed to specifically inhibit GSK-3 activity, i.e. GSK-3-specific chemical inhibitors, Wnt-3a conditioned media, small interfering RNAs, and GSK-3α and -3β kinase dead constructs, consistently showed that the levels of endogenous δ-catenin in CWR22Rv-1 prostate carcinoma cells and primary cortical neurons were increased by inhibiting GSK-3 activity. In addition, it was found that both GSK-3α and -3β interact with and phosphorylate δ-catenin. The phosphorylation of ΔC207-δ-catenin (lacking 207 C-terminal residues) and T1078A δ-catenin by GSK-3 was noticeably reduced compared with that of wild type δ-catenin, and the data from liquid chromatography-tandem mass spectrometry analyses suggest that the Thr¹⁰⁷⁸ residue of δ-catenin is one of the GSK-3 phosphorylation sites. Treatment with MG132 or ALLN, specific inhibitors of proteosome-dependent proteolysis, increased δ-catenin levels and caused an accumulation of ubiquitinated δ-catenin. It was also found that GSK-3 triggers the ubiquitination of δ-catenin. These results suggest that GSK-3 interacts with and phosphorylates δ-catenin and thereby negatively affects its stability by enabling its ubiquitination/proteosome-mediated proteolysis.δ-Catenin was first identified as a molecule that interacts with presenilin-1 (PS-1)² by yeast two-hybrid assay (1) and was found to belong to the p120-catenin subfamily of armadillo proteins, which characteristically contain 10 Arm repeats (2). In addition to its interaction with PS-1 and its abundant expression in brain (3, 4), several lines of evidence indicate that δ-catenin may play a pivotal role in cognitive function. First, the hemizygous loss of δ-catenin is known to be closely correlated with Cri-du-Chat syndrome, a severe form of mental retardation in humans (5). Second, severe learning deficits and abnormal synaptic plasticity were found in δ-catenin-deficient mice (6). Moreover, in δ-catenin^−/− mice, paired pulse facilitation (a form of short term plasticity) was found to be reduced, and long term potentiation, which is related to the forming and storage mechanisms of memory, was deficient (7, 8). Third, δ-catenin interacting molecules, such as PSs (1, 9), cadherins (10), S-SCAM (2), and PSD-95 (11), have been shown to play important roles in modulating synaptic plasticity. However, even though the maintenance of an adequate δ-catenin level is known to be critical for normal brain function, few studies have been undertaken to identify the factors that regulate δ-catenin stability in cells. We have previously demonstrated that PS-1 inhibits δ-catenin-induced cellular branching and promotes δ-catenin processing and turnover (12).Because of structural similarities among β-catenin, p120-catenin, and δ-catenin and to their shared binding partners (i.e. PS-1 (1, 9) and cadherins (10)), glycogen-synthase kinase-3 (GSK-3) drew our attention as a potential candidate effector of δ-catenin stability in cells. GSK-3 is a serine/threonine kinase and has two highly homologous forms, GSK-3α and GSK-3β, in mammals (13). Although GSK-3α and GSK-3β have similar structures, they differ in mass (GSK-3α (51 kDa) and GSK-3β (47 kDa) (13)) and to some extent in function (14). GSK-3 is a well established inhibitor of Wnt signaling. Moreover, it is known to phosphorylate β-catenin, which results in its degradation via ubiquitination/proteosome-dependent proteolysis (15). GSK-3 is ubiquitously distributed in the human body, but it is particularly abundant in brain (13), and it is interesting that δ-catenin is also abundant in the nervous system (4) and that GSK-3 participates in the progression of Alzheimer disease (16). The majority of GSK-3 substrates have the consensus sequence (Ser/Thr)-Xaa-Xaa-Xaa-(Ser/Thr) (17). Interestingly, we found that δ-catenin has several putative phosphorylation sites targeted by GSK-3, which suggests that δ-catenin can be regulated by GSK-3 in the same way as β-catenin.In this report, we demonstrate that both GSK-3α and -3β interact with and phosphorylate δ-catenin and that this leads to its subsequent ubiquitination and degradation via proteosome-dependent proteolysis. Our results strongly suggest that GSK-3 is a key regulator of δ-catenin stability in cells.     

利用ISSR标记研究野大豆居群内遗传变异及其取样策略

为了有效地保护野大豆(Glycine soja Sieb.et Zucc.)并制定合理的居群取样策略,对上海江湾机场的一个人然野大豆居群进行了 100个单株(个体)的随机取样,并用ISSR分子标记对其进行了遗传多样性分析.利用筛选出的15条ISSR引物在这个居群中检测到较高的遗传变异,样本内个体间的相似系数变化在0.17～0.89之间.居群内平均每个位点的平均预期杂合度(He)为0.171 4,香农指数(I)为0.271 4.PCA分析显示,江湾野大豆居群内的遗传变异不是呈均匀分布,而是呈从状分布.该野大豆居群遗传多样性和样本内个体数量间的相关性分析显示:在个体数少于40的情况下,遗传多样性随个体数的增加而迅速增加;当样本中的个体数大于40时,遗传多样性的增加减慢并很快趋于饱和.研究表明:对野大豆居群进行异地保护时,对各居群的采样植株数不应当低于35～45;在居群内采样时,所采集的个体之间最好相隔一定的空间距离.     

环境因子对植物释放挥发性化合物的影响

对近年来有关环境因子与植物释放挥发性化合物关系的研究进展进行了综合和概括。本文主要包括3类挥发性化合物。（1）异戊二烯是由叶绿体产生并且直接释放到大气中的C5化合物。（2）单萜类化合物是一类环状或非环状的C10化合物,它在植物体内合成后首先贮存于体内的特殊结构中（如树脂道、油腺）,然后由此通过气孔向大气中释放。（3）含氧挥发性化合物以各种形式释放到大气中。它包括醇、醛、酮、酯和有机酸。本文的重点是前两者, 主要阐述了二方面内容：(1)植物挥发性化合物的生物合成和释放机理。(2)环境因子（如温度、光照、水分胁迫、营养、CO2浓度、空气湿度）及植物的发育阶段、机械损伤和昆虫取食等对植物挥发性化合物合成与释放的影响机制。     

电子废物污染地区水生生物体内多氯联苯的异构体分布特征和毒性

电子废物已被证实是众多污染物的释放源,其引起的环境问题正日益受到人们的关注.利用同位素稀释GC/MS法测定了电子废物污染区的田螺、泥鳅和鲫鱼三种水生生物体内的PCBs含量和异构体组成特征.研究结果表明,田螺、泥鳅和鲫鱼体内PCBs平均浓度分别高达1303.53、3845.00和5645.34 ng/g脂重;毒性当量(TEQs)分别为1.35、8.44和29.18 pg WHO-TEQ/g湿重.其中,泥鳅和鲫鱼体内PCBs的TEQs都高于2006年欧盟规定的鱼类可食用部分最大TEQs允许值.此外,PCB 118是PCBs的主要异构体,分别占样品中PCBs总浓度和TEQs的57.73%-61.22%和44.27%-50.61%.而且,PCB 118与PCBs的总浓度和TEQs都具有良好的线性关系,相关系数(R2)分别为0.9988(P＜0.01)和0.9873(P＜0.01).这些研究结果表明,该地区的水生生物已经受到PCBs的严重污染,其体内的PCBs可能主要来自于电子废物拆解中释放的商业产品Aroelor 1254.     

常巢蛾属一新种记述(鳞翅目,巢蛾科)(英文)

记述了中国常巢蛾属Euhyponomeuta Toll,19411新种,即郑氏常巢蛾Euhyponomeuta zhengi sp.nov.,提供了新种的成虫及雄性外生殖器特征图。新种雄性外生殖器与圆腹常巢蛾E.rotunda Jin et Wang,2009相似,可通过尾突较宽且两侧平行、颚形突腹板宽舌状与其区分,后者尾突基部宽,端部渐窄,颚形突腹板三角形或半圆形。模式标本保存在南开大学生命科学学院昆虫标本室。     

呼伦贝尔草原沙狐洞穴的结构

沙狐（Vulpes corsac）又名东沙狐,属食肉目犬科,主要分布在亚洲中部的草原、荒漠和半荒漠地带,在我国主要分布在内蒙古、甘肃、宁夏和新疆部分地区。由于沙狐主要以鼠类为食,因此沙狐在调节鼠类数量和控制鼠害方面起着重要的作用（马逸清等,1986）。《中国物种红色名录》（汪松和解焱,2004）将沙狐列为“易危”,指出其“数据缺乏”。     

建立胃癌实验动物模型方法的研究

目的通过对人低分化胃癌细胞系SGC-7901状态和接种细胞数目的研究,建立良好的皮下接种胃癌的动物模型。方法采用腹腔注射SGC-7901细胞,使裸鼠形成腹水;光镜及电镜观察细胞状态;将购买的SGC-7901细胞以及形成腹水后的肿瘤细胞分别以1×108、1×107和1×106个进行裸鼠皮下接种,每组接种5只。观察其肿瘤形成时间、大小、状态及病理学变化。结果SGC-7901细胞接种裸鼠形成腹水后进行培养的肿瘤细胞增殖状态发生改变;购买的SGC-7901细胞以1×108及1×107接种裸鼠,在第21天肿瘤组织中央均出现出血和坏死;1×106的裸鼠第21天未见肉眼可见的肿瘤形成。腹水培养的肿瘤细胞,接种1×108的裸鼠在第21天肿瘤组织中央可见大面积的出血和坏死;接种1×107及1×106的裸鼠在第21天均未见出血和坏死,接种1×107的肿瘤组织体积较大。结论SGC-7901细胞接种裸鼠形成腹水后的细胞,更容易建立SGC-7901细胞皮下接种的胃癌动物模型,其中以接种细胞数为1×107的肿瘤生长较好,更适用于胃癌的实验研究。     

Using a non-radioisotopic, quantitative TRAP-based method detecting telomerase activities in human hepatoma cells

INTRODUCTIONTelomerase is a ribonucleoprotein complex that plays a critical role in telomeremaintenance and cellular immortality. Telomerase has been considered as tumordiagnostic marker and potential target for cancer therapyll, 2]. A sensitive, reliableand quantitative assay is of high interest in this field. The development of a very sensitive Telomeric Repeat Amplification Protocol (TRAP) for measuring telomerajseactivity in cell extracts has been proved to be an important tool for…