黑麦秸秆对土壤中无机氮转化和N_2O、CO_2释放的影响

在欧美国家,黑麦秸秆经常作为有机肥或农业废弃物而归还到农田中。本研究通过培养试验探讨了添加黑麦秸秆对土壤中无机氮的形态转化和N_2O、CO_2释放的影响。研究结果表明,黑麦秸秆的添加量及培养时间对土壤中N_2O、和CO_2释放量、N_2O/CO_2比值和无机氮形态转化均有明显影响。添加的黑麦秸秆越多,培养2周后土壤中的NH_4-N越多,释放的N_2O则越少。N_2O/CO_2比值与黑麦秸秆添加量呈极显著的负相关,与培养时间(T)的函数关系(达到极显著的负相关)则呈对数形式:(N_2O/CO_2)=a b·lnT。     

多效蒸发系统随机优化数学模型

提出了多效蒸发系统随机优化设计方法，并建了并流系统ＭｏｎｔｅＣａｒｌｏ优化数学模型。计算表明，最经济的多效蒸发系统，其各效蒸发面积往往是不相等的；价格体系对优化的结果有着直接的影响，能源价格越高，不等面积设计的优势就越大。     

关于电磁学中几个物理的矢量积分

对电磁学中几个矢量性物理量的矢量积分法进行了讨论，即比将矢量分解再行积分的方法简要，又突出了这些物理量本身的矢量性。     

基于鲁米诺的流动注射化学发光法测定硫酸链霉素

建立了一种简易、快速测定硫酸链霉素的流动注射化学发光法.本法基于在强碱性介质中,硫酸链霉素能增强铁氰化钾氧化鲁米诺产生化学发光,加入亚铁氰化钾能大大降低这一体系的背景发光强度.在优化的实验条件下该法测定硫酸链霉素的线性范围为5～1000μg/mL,检出限(3σ)为0 6μg/mL.对100μg/mL的硫酸链霉素进行11次平行测定,其RSD为2 2%.将本法用于硫酸链霉素制剂及合成样品的分析,结果令人满意.     

近0.5 ka来中国北方干旱半干旱地区的降水变化分析

从IGBP集成研究的思想出发, 采用冰芯、树轮、历史文献和湖泊沉积等多种气候代用资料, 重建了近0.5 ka来中国干旱区西部和东部, 以及整个干旱区分辨率为10年的降水变化序列. 在此基础上与1470年以来半干旱区西部和东部代用降水序列进行了比较. 结果表明, 近0.5 ka来各区域降水曲线均存在5次气候干旱期, 每个干旱期持续50年左右, 同时降水表现出区域差异性. 近0.5 ka来干旱区东部与半干旱区西部、半干旱区东部的降水呈现出基本一致的变化趋势, 而干旱区西部的降水变化比较独特, 呈现出显著的局地性降水特征. 最大熵谱和奇异谱分析结果表明每个区域降水序列, 包括干旱区西部、东部, 整个干旱区、半干旱区西部和东部, 以及中国北方区域降水序列, 均存在百年尺度约120年左右的周期.     

各向异性的气体-颗粒介质内的二通量辐射传热模型

二通量模型是计算气体-颗粒平板内辐射热通量的简化方法. 在最初的二通量模型中, 辐射场被假设成在半球方向的各向同性. 但是对于燃烧领域的气体-颗粒混合介质, 颗粒的散射通常都是各向异性的, 这样, 原有的二通量模型就会由于忽略各向异性而产生严重的误差. 文中一个多层四通量模型被运用到包含气体-颗粒混合物的辐射热通量的计算. 给出了模型的解析求解过程, 定义了等价的平均交叉系数h和前向散射率z来描述整个平板散射的各向异性. 为了验证模型的准确性, 计算了一个无限大平板内的辐射传递过程, 并与解析结果进行了比较. 结果表明提出的模型能够得到准确的结果, 对原有的二通量模型具有较好的改进作用. 运用本模型计算含有飞灰/CO₂/H₂O的燃烧产物的辐射传递, 所得到的平板发射率与Goodwin的经典结果相吻合.     

钢-混凝土预制混合梁受弯性能有限元分析

基于两端固定边界条件下钢-混凝土预制混合梁的受弯性能试验,采用ABAQUS软件对其受弯性能进行非线性有限元分析.通过与试验结果对比,验证了材料本构模型、单元类型、接触关系和边界条件等建模方法的可靠性.利用验证的有限元模型研究了钢梁长度以及钢梁与混凝土梁设计受弯承载力比对受弯性能的影响.结果表明:该有限元模型能有效地模拟钢-混凝土预制混合梁在静力集中荷载作用下的受弯性能;初始刚度随钢梁长度的增加呈线性降低;随着钢梁长度的增加,极限荷载先增后减,当钢梁长度超过400,mm后,极限荷载降低缓慢,钢梁所受最大弯矩基本保持不变.当钢梁长度为200~400,mm、钢梁与混凝土梁设计受弯承载力比为1.0~1.2时,钢梁强度可得到充分利用,且钢材用量相对较少.     

Experimental validation of inter-subspecific genetic diversity in rice represented by the differences between the DNA sequences of ‘Nipponbare’ and ‘93-11’

The pedigrees of three sequenced rice cultivars were analyzed to show that a majority of the genetic composition of 'Nipponbare' originates from japonica cultivars while the minority originates from indica cultivars. In contrast, '93-11' is derived mainly from indica cultivars with a smaller contribution from japonica cultivars. All ancestors of 'Guang lu ai 4' appeared to be indica lines. A set of molecular markers (46 InDels and 53 SSRs) polymorphic between 'Nipponbare' and '93-11' were examined in 46 typical indica and 47 typical japonica cultivars selected from 443 accessions according to Cheng's index. All cultivars were divided into indica and japonica groups without overlapping when clustered by Cheng's index, InDels and SSRs. Much higher InDel and SSR diversity between groups than within groups implies that the marker polymorphisms between 'Nipponbare' and '93-11' represent a large proportion of inter-subspecific diversity. About 85% of indica cultivars and more than 90% of japonica cultivars were confirmed to have the same PCR banding patterns as '93-11' and 'Nipponbare', respectively. Some polymorphic loci between 'Nipponbare' and '93-11' cannot be validated in other indica and japonica cultivars, either as subspecies-specific but not predominant alleles, or alleles not specific between the two groups. It was concluded that molecular markers developed from sequence polymorphism between 'Nipponbare' and '93-11' often represent inter-subspecific diversity, although some exceptions were sensitive to either particular marker loci or particular cultivars.     

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.     

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.