Glioma cell activation by Alzheimer's peptide Abeta1-42, alpha1-antichymotrypsin,and their mixture

We compared the effects ofAlzheimer's peptide (Abeta1-42), a,-antichymotrypsin (ACT) and an ACT/Abeta1-42 mixture on human glioma DK-MG cells. The solution of Abeta (5 microM) formed by 2-h incubation at room temperature induced tumour necrosis factor-alpha (TNF-alpha) and interleukin (IL)-6 levels by 55 and 45%, respectively, and increased gelatinase B activity by 67%, while exposure of cells to the ACT/Abeta1-42 mixture (1:10 molar ratio ACT: Abeta1-42) under the same experimental conditions showed no effect on IL-6 levels or gelatinase B activity, but strongly induced TNF-alpha (by 190%), compared to the controls. Stimulation of the cells with Abeta1-42 alone, but not with ACT, increased by about 20% low-density lipoprotein (LDL) uptake and mRNA levels for LDL receptor and HMG-CoA reductase, while the ACT/Abeta1-42 mixture significantly increased LDL uptake (by 50%), up-regulated mRNA levels for LDL receptor and HMG-CoA reductase by 48 and 63%, respectively, and increased lipid accumulation by about 20-fold. These data suggest a possible new role for Abeta in Alzheimer's disease through its interaction with the inflammatory reactant, ACT.     

一种用于结构动态过程数值模拟的广义有限元法

提出了一种能同时处理连续体和离散体动态过程的有限元法. 该法通过构造接触力模型, 将传统的离散元当做标准的一节点有限单元来看待. 新构造的一节点单元与常规有限单元具有同样物理特征, 包括应力和应变. 从而, 将离散元算法与有限元算法紧密结合在一起, 形成了统一的、与现有有限元系统兼容的广义有限元计算模型. 这种模型不仅简化了计算过程, 还可最大限度地发挥现有有限元代码的功能. 数值算例表明, 新方法可以更加有效地模拟大量离散体与连续体相互作用的复杂动力学过程.     

青藏高原北羌塘新生代火山岩黑云母地球化学及其岩石学意义

分析了北羌塘半岛湖新第三纪玻基粗面安山岩中黑云母的常量、微量及稀土元素特征.结果表明,黑云母均属钛铁黑云母类,富集大离子亲石元素Ba以及Sc,Ti,V,Cr,Co,Ni等铁族元素,而相对亏损Th,U,Pb等亲石元素.轻稀土强烈富集,轻重稀土分异显著,但Eu亏损并不严重,暗示原始岩浆来源于一个基性岩质的、相当于榴辉岩矿物相(斜长石相缺失)的源区类型.     

广西产眼镜王蛇毒α-神经毒素基因的分子克隆及序列分析

为获得眼镜王蛇（Ophiophagus hannah，简称Oh）蛇毒α－神经毒素（α-NT）的基因序列，依据眼镜蛇科不同毒蛇种类来源的α－NT基因有较高的同源性，设计1对上下游引物，为克服引物带来模糊扩增，在蛋白编码部分再设计1对上下游特异引物，用Nacleospin RNA Kit法从3条活眼镜王蛇毒腺中提取mRNA，以3′端引物合成的cDNA作为模板进行PCR扩增反应，测定产物的核苷酸序列，得到全长474bp的眼镜王蛇cDNA基因核苷酸序列。该核苷酸序列的信号肽与眼镜蛇树属Pseudonnaja textilis(Pt)、海蛇Laticauda semifasciata(Ls)100%同源，与眼镜蛇南洋亚种Naja sputatrix (Ns)、银环蛇（Bungarus multicinctus)(Bm)96.8%同源；蛋白密码部分有83．3％与Ns、79．2％与Pt、76．4％与Ls、74．1％与Bm同源。信号肽后紧接着的72个氨基酸有90．3％与已发现的眼镜王蛇毒长链α-NT Toxin a同源，大约有73．6％与Toxin b、69．7％与Oh-4、66．7％与Oh-5、56．9％与Oh-6A和6B同源，并与α－银环蛇毒素54．2％同源。说明新发现的眼镜王蛇cDNA是一条长链α-NT基因。     

Sox9 induces testis development in XX transgenic mice.

Mutations in SOX9 are associated with male-to-female sex reversal in humans. To analyze Sox9 function during sex determination, we ectopically expressed this gene in XX gonads. Here, we show that Sox9 is sufficient to induce testis formation in mice, indicating that it can substitute for the sex-determining gene Sry.     

Mutations in a human homologue of Drosophila crumbs cause retinitis pigmentosa (RP12).

Retinitis pigmentosa (RP) comprises a clinically and genetically heterogeneous group of diseases that afflicts approximately 1.5 million people worldwide. Affected individuals suffer from a progressive degeneration of the photoreceptors, eventually resulting in severe visual impairment. To isolate candidate genes for chorioretinal diseases, we cloned cDNAs specifically or preferentially expressed in the human retina and the retinal pigment epithelium (RPE) through a novel suppression subtractive hybridization (SSH) method. One of these cDNAs (RET3C11) mapped to chromosome 1q31-q32.1, a region harbouring a gene involved in a severe form of autosomal recessive RP characterized by a typical preservation of the para-arteriolar RPE (RP12; ref. 3). The full-length cDNA encodes an extracellular protein with 19 EGF-like domains, 3 laminin A G-like domains and a C-type lectin domain. This protein is homologous to the Drosophila melanogaster protein crumbs (CRB), and denoted CRB1 (crumbs homologue 1). In ten unrelated RP patients with preserved para-arteriolar RPE, we identified a homozygous AluY insertion disrupting the ORF, five homozygous missense mutations and four compound heterozygous mutations in CRB1. The similarity to CRB suggests a role for CRB1 in cell-cell interaction and possibly in the maintenance of cell polarity in the retina. The distinct RPE abnormalities observed in RP12 patients suggest that CRB1 mutations trigger a novel mechanism of photoreceptor degeneration.