富水泥岩大断面隧道开挖面稳定性及加固方式

富水泥岩隧道开挖过程中开挖面易失稳.以巴东隧道穿越富水紫红泥岩段为工程背景,基于岩土控制变形分析(ADECO-RS)及现场调查将开挖面稳定性评价为"C类稳定形态",提出超前帷幕注浆结合超前管棚的预加固措施.基于离散元方法构建泥岩隧道开挖模型,分析开挖面失稳过程及前方围岩变形破坏特征.结果 表明:开挖面失稳过程呈现"挤出变形-局部塌落-明显溜塌"的渐进破坏特性.发生溜塌后,开挖面前方拱部径向4.5m,纵向15 m范围松动区发育,孔(裂)隙率由0.1增至0.186;隧底出现相应范围的隆起区,颗粒接触力链分布稀疏,从宏细观层面进一步说明富水泥岩段开挖面前方失稳性强.考虑以上围岩扰动范围,提出了超前帷幕注浆参数,经现场应用,开挖面前方围岩加固效果良好,有效保证了大断面隧道施工安全,可为类似富水泥岩隧道设计、施工参考.     

多级齿轮装置热网络模型的拓扑建立

分析了多级齿轮装置热网络模型的建立方法，包括：机械结构的离散、网络的拓扑结构与数学描述．仿真与实验表明，模型可以准确地模拟减速器的热特性．     

Role for the nitrogenase MoFe protein alpha-subunit in FeMo-cofactor binding and catalysis

Two components constitute Mo-dependent nitrogenase (EC 1.18.6.1)--the Fe protein (a homodimer encoded by nifH) and the MoFe protein (an alpha 2 beta 2 tetramer encoded by nifDK). The MoFe protein provides the substrate-binding site and probably contains six prosthetic groups of two types--four Fe-S centres and two Fe- and Mo-containing cofactors. To determine the distribution and catalytic function of these metalloclusters, we and others are attempting to change the catalytic and spectroscopic features of nitrogenase by substituting specific amino acids targeted as potential metallocluster ligands, particularly those to the FeMo-cofactor, which is responsible for the biologically unique electron paramagnetic resonance signal (S = 3/2) of nitrogenase, and is believed to be the N2-reducing site. Here we describe mutant strains of Azotobacter vinelandii that have single amino-acid substitutions within the MoFe protein alpha-subunit. These substitutions alter both substrate-reduction properties and the unique electron paramagnetic resonance signal, indicating that the FeMo-cofactor is associated with both the alpha-subunit and the substrate-reducing site.     

Tenascin-X deficiency mimics Ehlers-Danlos syndrome in mice through alteration of collagen deposition

Tenascin-X is a large extracellular matrix protein of unknown function. Tenascin-X deficiency in humans is associated with Ehlers-Danlos syndrome, a generalized connective tissue disorder resulting from altered metabolism of the fibrillar collagens. Because TNXB is the first Ehlers-Danlos syndrome gene that does not encode a fibrillar collagen or collagen-modifying enzyme, we suggested that tenascin-X might regulate collagen synthesis or deposition. To test this hypothesis, we inactivated Tnxb in mice. Tnxb-/- mice showed progressive skin hyperextensibility, similar to individuals with Ehlers-Danlos syndrome. Biomechanical testing confirmed increased deformability and reduced tensile strength of their skin. The skin of Tnxb-/- mice was histologically normal, but its collagen content was significantly reduced. At the ultrastructural level, collagen fibrils of Tnxb-/- mice were of normal size and shape, but the density of fibrils in their skin was reduced, commensurate with the reduction in collagen content. Studies of cultured dermal fibroblasts showed that although synthesis of collagen I by Tnxb-/- and wildtype cells was similar, Tnxb-/- fibroblasts failed to deposit collagen I into cell-associated matrix. This study confirms a causative role for TNXB in human Ehlers-Danlos syndrome and suggests that tenascin-X is an essential regulator of collagen deposition by dermal fibroblasts.     

HZSM—23／γ—Al2O3丁烯异构化催化剂的活性和表面酸性

研究了ＨＺＳＭ－２３分子筛和γ－Ａｌ２Ｏ３配比对ＨＺＳＭ－２３／γ－Ａｌ２Ｏ３改性分子筛催化正丁烯异构化反应的转化率和选择性的影响．在中温及低空速条件下，随着配比中γ－Ａｌ２Ｏ３的增加，转化率降低而选择性有所提高．ＸＲＤ．ＴＰＤ及ＦＴ－ＩＲ对催化剂进行表征的结果显示：经改性后的ＨＺＳＭ－２３的总酸量和强酸位减少，而Ｌ酸的浓度增加，正丁烯异构化反应的选择性主要取决于Ｌ酸位浓度．     

Blindness and auditory impairment caused by loss of the sodium bicarbonate cotransporter NBC3

Normal sensory transduction requires the efficient disposal of acid (H+) generated by neuronal and sensory receptor activity. Multiple highly sensitive transport mechanisms have evolved in prokaryotic and eukaryotic organisms to maintain acidity within strict limits. It is currently assumed that the multiplicity of these processes provides a biological robustness. Here we report that the visual and auditory systems have a specific requirement for H+ disposal mediated by the sodium bicarbonate cotransporter NBC3 (refs. 7,8). Mice lacking NBC3 develop blindness and auditory impairment because of degeneration of sensory receptors in the eye and inner ear as in Usher syndrome. Our results indicate that in certain sensory organs, in which the requirement to transduce specific environmental signals with speed, sensitivity and reliability is paramount, the choice of the H+ disposal mechanism used is limited.     

配电系统可靠性数据统计与分析

本文以某市配电系统为主要研究对象，通过与国内外配电系统可靠性数据的对比，找出该配电系统在网络结构，设备可靠性及运行管理方面的不足，提出提高其可靠性的技术与管理措施。     

YBaCuO超导体的结构观测

本文报道我们对高Tc氧化物超导材料结构观测的结果。X射线能谱分析得到我们样品的成分为YBa_2Cu_3O_x,X值目前尚未测定。扫描电镜观测到,试样由大小不等的“块粒”物构成,块粒的典型尺寸为10μ。X射线衍射谱线分析证明样品接近单相,其主要相为钙钛矿型结构。透射电镜观测证明块粒为晶粒,但晶粒中有多种晶体缺陷,如孪晶,层错、位错等。     

Imprinting on distal chromosome 7 in the placenta involves repressive histone methylation independent of DNA methylation

Imprinted genes are expressed from only one of the parental chromosomes and are marked epigenetically by DNA methylation and histone modifications. The imprinting center 2 (IC2) on mouse distal chromosome 7 is flanked by several paternally repressed genes, with the more distant ones imprinted exclusively in the placenta. We found that most of these genes lack parent-specific DNA methylation, and genetic ablation of methylation does not lead to loss of their imprinting in the trophoblast (placenta). The silent paternal alleles of the genes are marked in the trophoblast by repressive histone modifications (dimethylation at Lys9 of histone H3 and trimethylation at Lys27 of histone H3), which are disrupted when IC2 is deleted, leading to reactivation of the paternal alleles. Thus, repressive histone methylation is recruited by IC2 (potentially through a noncoding antisense RNA) to the paternal chromosome in a region of at least 700 kb and maintains imprinting in this cluster in the placenta, independently of DNA methylation. We propose that an evolutionarily older imprinting mechanism limited to extraembryonic tissues was based on histone modifications, and that this mechanism was subsequently made more stable for use in embryonic lineages by the recruitment of DNA methylation.