系统发育史的重建

不同的物种是怎样进化形成不同的形态 ,这仍是现代进化生物学中研究的主要课题。近年来 ,对这一问题的研究已集中在由于进化时间的不同而导致进化机制变化的模型上 ,并在解开机体发育期间控制形态表现的分子机理方面取得了惊人的进展。值得注意的是 :形态的表型和一些调节基因的突变大致反映了物种间所表现的差异。通过分析生物的系统发育 ,重新构建系统发育史 ,可以阐明控制发育过程和进化发育的相关时间的遗传网络的分子进化机制。与系统发育进化有关的信息影印在组成它们的基因片段上。存在于这些发育位点的信息可以使人们追踪到发育调节…     

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。     

应用激光闪光法测量薄膜材料的热扩散率

目的是将用于测量片状试样的热扩散率的激光闪光法推广至测量薄膜试样。应用 1 5纳秒脉冲 Nd:YAG激光及响应时间 0 .9微秒的 (Hg,Cd) Te红外探测器等建立了闪光法热扩散率测量系统 ,并应用此系统对微米量级厚度的不锈钢薄膜进行了测量。同时针对将激光闪光法应用于薄膜时所出现的问题 ,如激光的有限脉冲时间及有限吸收厚度效应 ,测量系统的滞后效应 ,以及增强红外吸收及辐射用表面黑化膜的影响进行了分析并提出了解决方法     

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.     

Microbial desulfurization of fuel oil

Culture conditions of desulfurization microbes were investigated with a bioreactor controlled by computer.Factors such as pH, choice of carbon source, optimal concentrations of carbon, nitrogen and sulfur sources were determined. The addition of carbon in a culture with a constant pH greatly improved the growth of Rhodococcus. Cells and cell debris from microbes rested using a sulfur- specific pathway were used to desulfurize diesel oil treated by hydrodesulfurization (acquired from the Research Institute of Fushun Petroleum with total sulfur level at 205 μg/mL).Strains 1awq, IG, X7B, ZT, ZCR, and a mixture of No. 5 and No. 6, were used in the biodesulfurization process. The reduction of total sulfur was between 10.6% and 90.3%.     

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.     

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.