基于三角模型的机场拦阻功能评估

机场工程应用中,拦阻系统是飞机滑出跑道时的重要安全保障,评价拦阻系统功能的有效性与可靠性对保证飞机安全尤为必要。以舰载机拦阻索为主要研究对象,将拦阻系统在拦阻飞机过程中的具体功能分为阻碍功能、缓冲功能、导向功能等,分别对以上三项功能建立量化指标,采用函数分析方法确定不同指标量化数值,与权重组合得到相应指标评价值;最后结合三角图论构建模型对拦阻系统进行综合评价,分析拦阻系统功能变化趋势,确定具体评价结果。以某机场拦阻系统为例,收集拦阻过程各项数据进行实例分析。评价结果表明：利用所建立的拦阻功能评价方法,可得到拦阻系统在具体拦阻过程中的各项功能评价数值,其中拦阻系统阻碍功能、非缓冲功能、非导向功能所得值依次为0.83、0.46、0.64,根据结果对拦阻系统有效性和可靠性变化趋势做出判断。研究结果可为拦阻系统功能作用评估提供参考依据。     

基于统计损伤理论的饱和土邓肯-张修正模型

为了描述饱和土变形过程,以某边坡饱和土为研究对象,开展固结排水三轴压缩试验。试验发现饱和土的应力-应变曲线近似为双曲线,由此选择邓肯-张模型作为基础模型,结合统计损伤理论,构建一种新的饱和土邓肯-张修正模型。通过邓肯-张模型自身特性及线性回归的方法,求解模型参数。采用所建模型对饱和土试验数据进行辨识,对比分析试验曲线和理论曲线。结果表明,所建修正模型结构简练,参数较少,能较为准确地辨识饱和土偏应力-应变曲线,具有一定的可行性和合理性。     

基于响应面设计的头孢他啶母液冷冻浓缩工艺优化

以头孢他啶母液为原料,采用悬浮结晶冷冻浓缩技术回收头孢他啶母液中的有效成分。在单因素试验数据基础上,以头孢他啶回收率为评价指标,应用Box-Behnken响应面设计对冷冻温度、冷冻时间以及搅拌速率3个提取条件进行3因素3水平回归分析,优化最佳提取条件。得出头孢他啶最佳回收工艺条件为：冷冻温度－7 ℃,冷冻时间3 h,搅拌速率20 r/min。验证实验结果表明,此条件下头孢他啶回收率达到93.15%。结合生产实际情况优选的悬浮结晶冷冻浓缩工艺稳定,为头孢他啶的后续研究提供了一定的参考。     

Complex reorganization and predominant non-homologous repair following chromosomal breakage in karyotypically balanced germline rearrangements and transgenic integration

We defined the genetic landscape of balanced chromosomal rearrangements at nucleotide resolution by sequencing 141 breakpoints from cytogenetically interpreted translocations and inversions. We confirm that the recently described phenomenon of 'chromothripsis' (massive chromosomal shattering and reorganization) is not unique to cancer cells but also occurs in the germline, where it can resolve to a relatively balanced state with frequent inversions. We detected a high incidence of complex rearrangements (19.2%) and substantially less reliance on microhomology (31%) than previously observed in benign copy-number variants (CNVs). We compared these results to experimentally generated DNA breakage-repair by sequencing seven transgenic animals, revealing extensive rearrangement of the transgene and host genome with similar complexity to human germline alterations. Inversion was the most common rearrangement, suggesting that a combined mechanism involving template switching and non-homologous repair mediates the formation of balanced complex rearrangements that are viable, stably replicated and transmitted unaltered to subsequent generations.     

Mutations in the gene encoding pejvakin, a newly identified protein of the afferent auditory pathway, cause DFNB59 auditory neuropathy

Auditory neuropathy is a particular type of hearing impairment in which neural transmission of the auditory signal is impaired, while cochlear outer hair cells remain functional. Here we report on DFNB59, a newly identified gene on chromosome 2q31.1-q31.3 mutated in four families segregating autosomal recessive auditory neuropathy. DFNB59 encodes pejvakin, a 352-residue protein. Pejvakin is a paralog of DFNA5, a protein of unknown function also involved in deafness. By immunohistofluorescence, pejvakin is detected in the cell bodies of neurons of the afferent auditory pathway. Furthermore, Dfnb59 knock-in mice, homozygous for the R183W variant identified in one DFNB59 family, show abnormal auditory brainstem responses indicative of neuronal dysfunction along the auditory pathway. Unlike previously described sensorineural deafness genes, all of which underlie cochlear cell pathologies, DFNB59 is the first human gene implicated in nonsyndromic deafness due to a neuronal defect.     

Mitochondrial dysfunction and apoptosis in myopathic mice with collagen VI deficiency

Collagen VI is an extracellular matrix protein that forms a microfilamentous network in skeletal muscles and other organs. Inherited mutations in genes encoding collagen VI in humans cause two muscle diseases, Bethlem myopathy and Ullrich congenital muscular dystrophy. We previously generated collagen VI-deficient (Col6a1-/-) mice and showed that they have a muscle phenotype that strongly resembles Bethlem myopathy. The pathophysiological defects and mechanisms leading to the myopathic disorder were not known. Here we show that Col6a1-/- muscles have a loss of contractile strength associated with ultrastructural alterations of sarcoplasmic reticulum (SR) and mitochondria and spontaneous apoptosis. We found a latent mitochondrial dysfunction in myofibers of Col6a1-/- mice on incubation with the selective F1F(O)-ATPase inhibitor oligomycin, which caused mitochondrial depolarization, Ca2+ deregulation and increased apoptosis. These defects were reversible, as they could be normalized by plating Col6a1-/- myofibers on collagen VI or by addition of cyclosporin A (CsA), the inhibitor of mitochondrial permeability transition pore (PTP). Treatment of Col6a1-/- mice with CsA rescued the muscle ultrastructural defects and markedly decreased the number of apoptotic nuclei in vivo. These findings indicate that collagen VI myopathies have an unexpected mitochondrial pathogenesis that could be exploited for therapeutic intervention.     

形变双奇核1944Au中的强耦合带

利用重离子融合蒸发反应159Tb（29Si,4nγ）194Au布居了形变双奇核184Au的高自旋态,用GASP探测器阵列进行了在束γ实验测量．通过对实验数据的深入分析,新发现了一条可归属于184Au核的强耦合转动带．基于对转动带有效K值的分析以及从实验数据中提取出的带内B（M1）／B（E2）值与理论计算值的比较,建议了转动带的准粒子组态和能级的自旋宇称值．     

利用人工智能神经网络和DEM数据进行植被变化探测

适时精确的探测土地利用和覆盖变化是研究其起因、过程和效应的基础.本研究利用人工智能神经网络对两景不同时期的影像(2003和2004年)进行一次性变化探测.并且输入层中增加了DEM和坡度两个额外"波段".在选取训练样区的过程中,共选取了82个亚类型,其中36个为植被变化亚类型,46个为无变化植被亚类型.NDVI差值法被用于探测变化和无变化的区域,该方法为获取精确的和足够的植被变化类型训练样区提供有效的参考.研究结果显示利用人工智能神经网络探测变化技术所产生的植被变化图,其精度明显高于分类后比较法所产生的植被变化图精度.此外将DEM和坡度作为额外波段结合两景影像得的8个主成分作为输入层,能够有效的提高人工智能神经网络进行山区植被变化探测精度.同时在选取训练样区的过程中,将各不同的变化和无变化的植被类型根据其不同的光谱特征分成不同的亚类型进行取样,对提高人工智能神经网络进行山区植被变化探测精度有着非常重要的促进作用,此处理可以降低山区影像的地形效应.     

珠江流域盆地表层沉积物的黏土矿物及其对南海沉积物的贡献

黏土矿物以其示踪洋流变化和揭示物源区陆地同时期气候变化的能力, 近年来在南海东亚季风演化的研究中起到了重要作用. 珠江作为南海北部陆源物质输入的重要河流之一, 以往的研究还没有开展过详细的黏土矿物学工作. 运用X射线衍射方法, 系统地研究了珠江流域盆地(包括珠江主流、各支流和珠江口伶仃洋)表层沉积物的黏土矿物组合. 结果显示, 珠江流域盆地黏土矿物组合主要由高岭石(35%~65%)、绿泥石(20%~35%)和伊利石(12%~42%)组成, 蒙脱石含量一般小于5%, 区域分布上不具明显的差异性. 但是, 从珠江流域盆地到南海北部, 高岭石含量持续降低, 蒙脱石含量持续上升, 伊利石含量也不断上升, 伊利石化学指数递减, 伊利石结晶度增强, 这些特征都表明珠江流域盆地对南海北部黏土矿物的贡献主要是高岭石, 其次是伊利石和绿泥石, 基本不提供蒙脱石. 研究认为, 珠江对南海北部陆缘的黏土矿物贡献率最多为72%, 而对北部陆坡的贡献率最多仅为15%. 无论是冰期还是间冰期时期, 高岭石都指示了珠江流域的机械侵蚀能力.