中国北方表土微团粒粒度分布及其对粉尘

利用干筛筛析法测定了中国北方沙漠、戈壁、绿洲、干草原农垦区和草原牧区等代表性表土(沙质土、砾质沙土、砾质壤土、壤土和粉壤土等)的微团粒粒度分布. 组成表土微团粒粒度分布的对数正态群体分别为粉细沙、细沙、中沙、粗沙和极粗沙群体, 其平均的质量中值粒径分别为90, 210, 390, 600和980 mm, 平均的标准偏差分别为1.25, 1.40, 1.25, 1.35和1.25. 粉细沙、细沙、中沙、粗沙、砾质沙、砾质壤土、壤土等表土类型的微团粒粒度分布为这几个对数正态分布群体中的组合. 粉尘释放模型(DPM模型)模拟的结果显示: 表土微团粒粒度分布对粉尘释放通量存在显著影响, 细沙和粉细沙的粉尘释放通量最大, 中沙、砾质沙、砾质壤土、壤土、粉壤土次之, 粗沙的粉尘通量最小, 差值范围在10¹~10³ mg·m^-2·s^-1左右; 中国北方沙漠(沙地)和片状流沙覆盖的农田的粉尘释放通量在10¹~10⁴ mg· m^-2·s^-1之间, 而沙砾质戈壁、沙砾质化的农田和草原的粉尘释放通量在10¹~10² mg·m^-2·s^-1之间, 表明中国北方沙漠(沙地)和片状流沙覆盖的农田是粉尘释放的主要源地.     

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.     

新型层状农药缓/控释材料—草甘膦插层双金属氢氧化物的超分子结构与缓释性能

以镁铝双金属氢氧化物(MgAl layered double hydroxide: MgAl-LDH)为主体, 以草甘膦(Glyphosate: GLY)为客体, 通过控制反应pH值, 由共沉淀法组装得到两种不同结构的GLY插层MgAl-LDH缓/控释材料. 考察了该缓/控释材料在Na₂CO₃溶液中的缓释性能, 其缓释历程为客体阴离子与介质中CO₃^2-的离子交换过程, 客体阴离子在插层化合物层间及晶粒间隙的扩散, 即粒内扩散过程为释放速率控制步. 低pH合成GLY插层产物较大的层间距、层间客体GLY阴离子单层垂直的定位方向及较高的堆积密度使其较高pH合成材料展示出更为显著的缓释能力, 其原因归结为超分子结构对释放速率控制步的影响. 该研究指出了层状双金属氢氧化物在农药缓/控释领域的应用潜力.     

Nanoengineering of amino - functionalized mesoporous silica nanospheres as nanoreactors

Selective functionalization of mesoporous silica nanospheres (MSNs) is crucial for nanoengineering of MSNs. Herein, we have combined “surface-protected etching strategy” and “cationic surfactant assisted etching strategy” to prepare functionalized MSNs with externally attached amino groups. The externally attached NH2 groups endow the catalysts with excellent catalytic performance for nitroaldol reaction between nitromethane and benzaldehyde. In addition, those NH2-MSNs can also be used to support gold nanoparticles, which display very good catalytic performance for reduction of 4-nitrophenol. It can be envisioned that the synthesis protocol developed in this work could also be extended to nanoengineered MSNs, which provides opportunities for nanoreactors design.     

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.     

Heritable and inducible genetic interference by double-stranded RNA encoded by transgenes

Double-stranded RNA interference (RNAi) is an effective method for disrupting expression of specific genes in Caenorhabditis elegans and other organisms. Applications of this reverse-genetics tool, however, are somewhat restricted in nematodes because introduced dsRNA is not stably inherited. Another difficulty is that RNAi disruption of late-acting genes has been generally less consistent than that of embryonically expressed genes, perhaps because the concentration of dsRNA becomes lower as cellular division proceeds or as developmental time advances. In particular, some neuronally expressed genes appear refractory to dsRNA-mediated interference. We sought to extend the applicability of RNAi by in vivo expression of heritable inverted-repeat (IR) genes. We assayed the efficacy of in vivo-driven RNAi in three situations for which heritable, inducible RNAi would be advantageous: (i) production of large numbers of animals deficient for gene activities required for viability or reproduction; (ii) generation of large populations of phenocopy mutants for biochemical analysis; and (iii) effective gene inactivation in the nervous system. We report that heritable IR genes confer potent and specific gene inactivation for each of these applications. We suggest that a similar strategy might be used to test for dsRNA interference effects in higher organisms in which it is feasible to construct transgenic animals, but impossible to directly or transiently introduce high concentrations of dsRNA.     

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.