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.     

音乐的结构及其数字人类学根据

音乐作为一种纯粹的文化制度,有其固有的结构和强加的结构。音乐结构原理的应用有力地说明,音乐有其明确规定的数字人类学根据。     

最后的巡航——苏联K-219战略核潜艇沉没揭秘

1986年10月3日,苏联K-219号战略导弹核潜艇在美国东海岸附近沉没。次日,塔斯社发表通告:“苏联核潜艇在百慕大群岛东北约1000公里海域执行任务时隔舱起火,艇上部分官兵遇难……。”第十三次战斗巡航1986年9月,苏联Y级667АУ型战略导弹核潜艇K-219号从巴伦支海出发前往大西洋担     

国际单项体育联合会善治评价体系构建及其实证研究

基于治理理论和委托—代理模型,本研究以35 个国际单项体育联合会善治 评价为对象,设计了以透明度、程序民主、制衡、团结等维度作为关键维度的指标体系, 并使用文献资料法、问卷调查法和访谈法等方法,对数据进行搜集整理。研究发现,国 际单项体育联合会平均得分为45.5（满分100）,善治状况评价为“一般”,决策和工作 机制不透明、选举和工作程序失范、利益相关者参与不足等,导致组织内部投机主义盛 行,国际单项体育联合会合法性面临危机。研究建议：1）严格执行选举程序,健全主席 和高管资格审查机制;2）完善信息公开制度,提升组织透明度;3）规范工作流程,充 实组织行政程序正当性;4）多元主体参与,健全组织内外部审查制度;5）明确最长任 期,保证组织官员积极性。     

新疆哈萨克羊NYD-SP27基因的克隆及序列分析

本研究通过新疆哈萨克羊NYD-SP27基因的克隆及序列分析,为研究绵羊NYD-SP27表达调控机制奠定基础。根据Genbank中公布的人类的NYD-SP27基因序列设计引物,本研究以新疆哈萨克羊的睾丸组织的总DNA为模板,采用RT-PCR扩增方法对绵羊NYD-SP27基因序列进行研究。结果显示:哈萨克羊NYD-SP27基因全长为1901 bp,其中只含有1617 bp组成的开放阅读框(ORF),共编码538个氨基酸;相对分子质量61995.66,理论PI值为6.16,正电荷残基数(Arg+Lys)为61,负电荷残基数(Asp+Glu)为67;分子式C2798H4319N737O819S19;体外半衰期为30 h,不稳定系数46.96(不稳定);总平均吸水性-0.403。结论:哈萨克羊NYD-SP27基因属于PLCζ家族;同时将所得序列已提交到Gene Bank(登录号:KX905090)。     

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.