非光滑表面离心泵叶轮的流动减阻特性

为了分析非光滑表面对离心泵性能的影响,基于仿生凹坑表面的减阻特性,将凹坑型非光滑单元体排布于离心泵叶片的工作面,建立具有非光滑表面的叶轮离心泵的流动减阻特性分析模型,通过RNGk-ε湍流模型对离心泵内部流场进行数值模拟,分析具有非光滑表面叶轮的流动减阻特性,研究不同流量下非光滑表面对叶片近壁面的速度分布、剪应力和离心泵内部流场的影响.结果表明:凹坑型非光滑表面能够降低因黏性阻力产生的叶轮扭矩,其扭矩的最大降幅为5.8%;非光滑表面能够有效控制叶片近壁面边界层的流体流动,减小叶片的壁面剪应力;凹坑型非光滑表面能够降低离心泵叶轮内部流体的湍动程度,减小湍动产生的能量耗散,使叶轮内部的流体流动更加稳定并提高离心泵的效率.     

High foal mortality limits growth of a desert feral horse population in Nevada

A population of feral horses ( Equus caballus ) in the southern Great Basin Desert of Nevada was monitored from 1989 to 1998 to determine size, distribution, and population trends. All individual horses observed in the population were identified by unique markings during the first 2 yr of study, and most animals could be observed annually. During this study no new horses were identified in the population, indicating that no immigration occurred from outside populations. The population reached a high of 65 horses yearling or older in 1992 and declined each year thereafter, reaching a low of 36 horses in 1998. Estimated foal survival averaged < 12% over 8 yr. Only 11 horses were recruited into the population as yearlings or older animals during the study. Mountain lion predation is hypothesized as major factor limiting growth of this feral horse population.     

Discovery of previously unidentified genomic disorders from the duplication architecture of the human genome

Genomic disorders are characterized by the presence of flanking segmental duplications that predispose these regions to recurrent rearrangement. Based on the duplication architecture of the genome, we investigated 130 regions that we hypothesized as candidates for previously undescribed genomic disorders. We tested 290 individuals with mental retardation by BAC array comparative genomic hybridization and identified 16 pathogenic rearrangements, including de novo microdeletions of 17q21.31 found in four individuals. Using oligonucleotide arrays, we refined the breakpoints of this microdeletion, defining a 478-kb critical region containing six genes that were deleted in all four individuals. We mapped the breakpoints of this deletion and of four other pathogenic rearrangements in 1q21.1, 15q13, 15q24 and 17q12 to flanking segmental duplications, suggesting that these are also sites of recurrent rearrangement. In common with the 17q21.31 deletion, these breakpoint regions are sites of copy number polymorphism in controls, indicating that these may be inherently unstable genomic regions.     

Structural diversity and African origin of the 17q21.31 inversion polymorphism

The 17q21.31 inversion polymorphism exists either as direct (H1) or inverted (H2) haplotypes with differential predispositions to disease and selection. We investigated its genetic diversity in 2,700 individuals, with an emphasis on African populations. We characterize eight structural haplotypes due to complex rearrangements that vary in size from 1.08-1.49 Mb and provide evidence for a 30-kb H1-H2 double recombination event. We show that recurrent partial duplications of the KANSL1 gene have occurred on both the H1 and H2 haplotypes and have risen to high frequency in European populations. We identify a likely ancestral H2 haplotype (H2') lacking these duplications that is enriched among African hunter-gatherer groups yet essentially absent from West African populations. Whereas H1 and H2 segmental duplications arose independently and before human migration out of Africa, they have reached high frequencies recently among Europeans, either because of extraordinary genetic drift or selective sweeps.     

A copy number variation morbidity map of developmental delay

To understand the genetic heterogeneity underlying developmental delay, we compared copy number variants (CNVs) in 15,767 children with intellectual disability and various congenital defects (cases) to CNVs in 8,329 unaffected adult controls. We estimate that ～14.2% of disease in these children is caused by CNVs >400 kb. We observed a greater enrichment of CNVs in individuals with craniofacial anomalies and cardiovascular defects compared to those with epilepsy or autism. We identified 59 pathogenic CNVs, including 14 new or previously weakly supported candidates, refined the critical interval for several genomic disorders, such as the 17q21.31 microdeletion syndrome, and identified 940 candidate dosage-sensitive genes. We also developed methods to opportunistically discover small, disruptive CNVs within the large and growing diagnostic array datasets. This evolving CNV morbidity map, combined with exome and genome sequencing, will be critical for deciphering the genetic basis of developmental delay, intellectual disability and autism spectrum disorders.     

Inherited semisterility for control of harmful insects. V. Translocations inCulex tritaenio-rhynchus

Zusammenfassung Mit unterschiedlichen Dosen von Röntgenstrahlen wurden bei der StechmückeCulex tritaeniorhynchus chromosomale Aberrationen (vorwiegend reziproke Translokationen) produziert, die von der zweiten Tochtergeneration an einen konstanten Grad von Semisterilität zeigen. Die Mehrzahl der isolierten Linien zeigte im Durchschnitt eine Letalität von etwa 50%. Die Variationsbreite innerhalb einer Linie betrug ±10–15%. Durch cytologische Untersuchungen von Prophasechromosomen wurden die geschlechtsbestimmenden Faktoren M und m auf einem der beiden langen Chromosomen lokalisiert.     

Induction of c-fos-like protein in spinal cord neurons following sensory stimulation

It has been suggested that the proto-oncogenes c-fos and c-myc participate in the control of genetic events which lead to the establishment of prolonged functional changes in neurons. Expression of c-fos and c-myc are among the earliest genetic events induced in cultured fibroblast and phaeochromocytoma cell lines by various stimuli including growth factors, peptides and the intracellular second messengers diacylglycerol, cAMP and Ca2+. We report here that physiological stimulation of rat primary sensory neurons causes the expression of c-fos-protein-like immunoreactivity in nuclei of postsynaptic neurons of the dorsal horn of the spinal cord. Activation of small-diameter cutaneous sensory afferents by noxious heat or chemical stimuli results in the rapid appearance of c-fos-protein-like immunoreactivity in the superficial layers of the dorsal horn. However, activation of low-threshold cutaneous afferents results in fewer labelled cells with a different laminar distribution. No c-fos induction was seen in the dorsal root ganglia, gracile nucleus or ventral horn. Thus, synaptic transmission may induce rapid changes in gene expression in certain postsynaptic neurons.