合并财务报表中合并范围的确定

首先介绍了判断控制的两种标准：定量标准与定性标准，然后通过分析使用定量标准确定合并范围的不足，得出合并范围的确定庆以定性标准为主，定量标准为辅的结论。并构造了流程图来说明两种标准的具体应用。     

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。     

Superoxide activates mitochondrial uncoupling proteins.

Uncoupling protein 1 (UCP1) diverts energy from ATP synthesis to thermogenesis in the mitochondria of brown adipose tissue by catalysing a regulated leak of protons across the inner membrane. The functions of its homologues, UCP2 and UCP3, in other tissues are debated. UCP2 and UCP3 are present at much lower abundance than UCP1, and the uncoupling with which they are associated is not significantly thermogenic. Mild uncoupling would, however, decrease the mitochondrial production of reactive oxygen species, which are important mediators of oxidative damage. Here we show that superoxide increases mitochondrial proton conductance through effects on UCP1, UCP2 and UCP3. Superoxide-induced uncoupling requires fatty acids and is inhibited by purine nucleotides. It correlates with the tissue expression of UCPs, appears in mitochondria from yeast expressing UCP1, and is absent in skeletal muscle mitochondria from UCP3 knockout mice. Our findings indicate that the interaction of superoxide with UCPs may be a mechanism for decreasing the concentrations of reactive oxygen species inside mitochondria.     

完全图Kn和完全多部图Kn(t)的{C3,S4}-强制分解

本文给出完全图Kn和完全多部图Kn(t)存在{C3, S4}-强制分解的充分必要条件.     

Don't mess with the matrix.

Extracellular matrix (ECM) remodeling is critical to morphogenesis and homeostasis. The identification of inactivating mutations in a gene encoding one of its modifying enzymes, matrix metalloproteinase 2 (MMP-2), in people with a hereditary disorder in which the bones disintegrate, represents the first genetic evidence that the proteolysis of the ECM mediates human growth and development. It also underscores the need for an intricate balance between breakdown and deposition of the ECM.     

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.     

改良型9Cr-1Mo钢的形变热处理强化机制

采用形变热处理技术有效地提高改良型T91 耐热钢的高温回火抗力和室温综合力学性能。该钢经形变热处理后性能提高的主要机制是细晶强化和伴随晶粒细化而产生的马氏体组织的细化以及析出物的弥散分布。