次序统计量分布的参数识别

设x_1,x_2,…,x_n是n个相互独立的随机变量,第k个(1≤k≤n)次序统计量x(k)的分布是否能唯一决定每个随机变量x_i(i=1,2,…,n)的分布,当k=n时,Anderson TW等对一定类型的随机变量作出了肯定的回答。本文将对一定类型的相互独立同分布(i.i.d.)的随机变量,研究k为任意正整数(1≤k≤n)时上述提出的问题。     

Dynamics of seismogenic volcanic extrusion at Mount St Helens in 2004-05

The 2004-05 eruption of Mount St Helens exhibited sustained, near-equilibrium behaviour characterized by relatively steady extrusion of a solid dacite plug and nearly periodic shallow earthquakes. Here we present a diverse data set to support our hypothesis that these earthquakes resulted from stick-slip motion along the margins of the plug as it was forced incrementally upwards by ascending, solidifying, gas-poor magma. We formalize this hypothesis with a dynamical model that reveals a strong analogy between behaviour of the magma-plug system and that of a variably damped oscillator. Modelled stick-slip oscillations have properties that help constrain the balance of forces governing the earthquakes and eruption, and they imply that magma pressure never deviated much from the steady equilibrium pressure. We infer that the volcano was probably poised in a near-eruptive equilibrium state long before the onset of the 2004-05 eruption.     

A HEURISTIC PATH-PLANNING METHOD FOR ENHANCING MACHINE-TOOL CONTOUR-FOLLOWING

Nomenclature ki integral action coefficient[s-1]kp speed proportional gain[s-1]kv position proportional gain[s-1]kf feed forward factor of the speed loop[%]M axis mass[kg]V speed[m/s]F driving effort[N]Rc radius of curvature[m]d distance to the apex[m]o lateral offset[m]εcontouring error[m]ωm lowest mechanical resonant frequency[s-1]ζdamping coefficient[-]r inertia ratio[-]μmembership function[-]αcorner angle[rad]x,y horizontal and vertical coordinates[m]?angle to the normal line[rad]1.I…     

Ru2 and Ru encode mouse orthologs of the genes mutated in human Hermansky-Pudlak syndrome types 5 and 6

Hermansky-Pudlak syndrome (HPS) is a genetically heterogeneous disease involving abnormalities of melanosomes, platelet dense granules and lysosomes. Here we have used positional candidate and transgenic rescue approaches to identify the genes mutated in ruby-eye 2 and ruby-eye mice (ru2 and ru, respectively), two 'mimic' mouse models of HPS. We also show that these genes are orthologs of the genes mutated in individuals with HPS types 5 and 6, respectively, and that their protein products directly interact. Both genes are previously unknown and are found only in higher eukaryotes, and together represent a new class of genes that have evolved in higher organisms to govern the synthesis of highly specialized lysosome-related organelles.     

Mutations in SEC63 cause autosomal dominant polycystic liver disease

Mutations in PRKCSH, encoding the beta-subunit of glucosidase II, an N-linked glycan-processing enzyme in the endoplasmic reticulum (ER), cause autosomal dominant polycystic liver disease. We found that mutations in SEC63, encoding a component of the protein translocation machinery in the ER, also cause this disease. These findings are suggestive of a role for cotranslational protein-processing pathways in maintaining epithelial luminal structure and implicate noncilial ER proteins in human polycystic disease.     

Three-dimensional brittle shear fracturing by tensile crack interaction

Faults in brittle rock are shear fractures formed through the interaction and coalescence of many tensile microcracks. The geometry of these microcracks and their surrounding elastic stress fields control the orientation of the final shear fracture surfaces. The classic Coulomb-Mohr failure criterion predicts the development of two conjugate (bimodal) shear planes that are inclined at an acute angle to the axis of maximum compressive stress. This criterion, however, is incapable of explaining the three-dimensional polymodal fault patterns that are widely observed in rocks. Here we show that the elastic stress around tensile microcracks in three dimensions promotes a mutual interaction that produces brittle shear planes oriented obliquely to the remote principal stresses, and can therefore account for observed polymodal fault patterns. Our microcrack interaction model is based on the three-dimensional solution of Eshelby, unlike previous models that employed two-dimensional approximations. Our model predicts that shear fractures formed by the coalescence of interacting mode I cracks will be inclined at a maximum of 26 degrees to the axes of remote maximum and intermediate compression. An improved understanding of brittle shear failure in three dimensions has important implications for earthquake seismology and rock-mass stability, as well as fluid migration in fractured rocks.     

The Ter mutation in the dead end gene causes germ cell loss and testicular germ cell tumours

In mice, the Ter mutation causes primordial germ cell (PGC) loss in all genetic backgrounds. Ter is also a potent modifier of spontaneous testicular germ cell tumour (TGCT) susceptibility in the 129 family of inbred strains, and markedly increases TGCT incidence in 129-Ter/Ter males. In 129-Ter/Ter mice, some of the remaining PGCs transform into undifferentiated pluripotent embryonal carcinoma cells, and after birth differentiate into various cells and tissues that compose TGCTs. Here, we report the positional cloning of Ter, revealing a point mutation that introduces a termination codon in the mouse orthologue (Dnd1) of the zebrafish dead end (dnd) gene. PGC deficiency is corrected both with bacterial artificial chromosomes that contain Dnd1 and with a Dnd1-encoding transgene. Dnd1 is expressed in fetal gonads during the critical period when TGCTs originate. DND1 has an RNA recognition motif and is most similar to the apobec complementation factor, a component of the cytidine to uridine RNA-editing complex. These results suggest that Ter may adversely affect essential aspects of RNA biology during PGC development. DND1 is the first protein known to have an RNA recognition motif directly implicated as a heritable cause of spontaneous tumorigenesis. TGCT development in the 129-Ter mouse strain models paediatric TGCT in humans. This work will have important implications for our understanding of the genetic control of TGCT pathogenesis and PGC biology.     

Corneal avascularity is due to soluble VEGF receptor-1

Corneal avascularity-the absence of blood vessels in the cornea-is required for optical clarity and optimal vision, and has led to the cornea being widely used for validating pro- and anti-angiogenic therapeutic strategies for many disorders. But the molecular underpinnings of the avascular phenotype have until now remained obscure and are all the more remarkable given the presence in the cornea of vascular endothelial growth factor (VEGF)-A, a potent stimulator of angiogenesis, and the proximity of the cornea to vascularized tissues. Here we show that the cornea expresses soluble VEGF receptor-1 (sVEGFR-1; also known as sflt-1) and that suppression of this endogenous VEGF-A trap by neutralizing antibodies, RNA interference or Cre-lox-mediated gene disruption abolishes corneal avascularity in mice. The spontaneously vascularized corneas of corn1 and Pax6+/- mice and Pax6+/- patients with aniridia are deficient in sflt-1, and recombinant sflt-1 administration restores corneal avascularity in corn1 and Pax6+/- mice. Manatees, the only known creatures uniformly to have vascularized corneas, do not express sflt-1, whereas the avascular corneas of dugongs, also members of the order Sirenia, elephants, the closest extant terrestrial phylogenetic relatives of manatees, and other marine mammals (dolphins and whales) contain sflt-1, indicating that it has a crucial, evolutionarily conserved role. The recognition that sflt-1 is essential for preserving the avascular ambit of the cornea can rationally guide its use as a platform for angiogenic modulators, supports its use in treating neovascular diseases, and might provide insight into the immunological privilege of the cornea.