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This paper uses the Oseen transformation to solve the differential equations governing motion of the vertical linear gradient flow distribution close to a wall surface. The Navier-Stokes equations are used to consider the inertia term along the flow direction. A novel contour integral method is used to solve the complex Airy function. The boundary conditions of linear gradient flow distribution for finite problems are determined. The vorticity function, the pressure function, and the turbulent velocity profiles are provided, and the stability of particle trajectories is studied. An L-function form of the third derivative circulation is used to to simplify the solution. Theoretical results are compared with the experimental measurements with satisfactory agreement. [ABSTRACT FROM AUTHOR]

With some popular tracking methods for free surface, simulations of several typical examples are carried out under various flow field conditions. The results show that the Smoothed Particle Hydrodynamics (SPH) method is very suitable in simulating the flow problems with a free surface. A viscous liquid droplet with an initial velocity impacting on a solid surface is simulated based on the SPH method, and the surface tension is considered by searching the free surface particles, the initial impact effect is considered by using the artificial viscosity method, boundary virtual particles and image virtual particles are introduced to deal with the boundary problem, and the boundary defect can be identified quite well. The comparisons of simulated results and experimental photographs show that the SPH method can not only exactly simulate the spreading process and the rebound process of a liquid droplet impacting on a solid surface but also accurately track the free surface particles, simulate the free-surface flow and determine the shape of the free surface due to its particle nature. [ABSTRACT FROM AUTHOR]

Through the study of the theory of oil spill model, a mathematical modeling of oil spill on the sea is developed which with the consideration of spread, diffusion, drifting and attenuation of oil slick is influenced by evaporation and emulsification factors. A model that under the effect of ocean dynamic condition of tide, wind and wave, using Monte Carlo method to simulate the movement of oil slick is established. The modeling is applied to calculate and predict pollution range of oil spill at oil quay and oil ship in Daya Bay. The prediction results have basically shown the pollution situation by emergency of oil spill on the sea. [ABSTRACT FROM AUTHOR]

ABSTRACT: The risk analysis of urban rainstorm water logging facing Tianjin city by using methods of probability, investigation and numerical simulation was carried out in this article. Firstly, a mathematical model for the urban rainstorm water logging was established on the basis of one- and two-dimensional unsteady flow theory and the technique of non-structural irregular grid division, Secondly, the precipitation over heavy rain was divided into seven grades, the experiential expression of frequency and rain grades was got according to the observed rainfall from May 1918 to October 1998. Thirdly, the mathematical model was used to simulate various rain process according to the features of the rainstorm and the draining rule, based on the simulated maximum water depths, 3 class of disaster extents were established, the disaster risks were mainly in Class I and Class II, The risk analysis of water logging on traffic were primarily evaluated, and finally, some management and mitigation measures of the urban rainstorm water logging disaster were discussed. [Copyright &y& Elsevier]

ABSTRACT: The risk analysis of urban rainstorm water logging facing Tianjin city by using methods of probability, investigation and numerical simulation was carried out in this article. Firstly, a mathematical model for the urban rainstorm water logging was established on the basis of one- and two-dimensional unsteady flow theory and the technique of non-structural irregular grid division, Secondly, the precipitation over heavy rain was divided into seven grades, the experiential expression of frequency and rain grades was got according to the observed rainfall from May 1918 to October 1998. Thirdly, the mathematical model was used to simulate various rain process according to the features of the rainstorm and the draining rule, based on the simulated maximum water depths, 3 class of disaster extents were established, the disaster risks were mainly in Class I and Class II, The risk analysis of water logging on traffic were primarily evaluated, and finally, some management and mitigation measures of the urban rainstorm water logging disaster were discussed. [Copyright &y& Elsevier]

LATS (large tumour suppressor) is a family of conserved tumour suppressors identified in Drosophila and mammals. Here we show that human LATS1 binds to LIMK1 in vitro and in vivo and colocalizes with LIMK1 at the actomyosin contractile ring during cytokinesis. LATS1 inhibits both the phosphorylation of cofilin by LIMK1 and LIMK1-induced cytokinesis defects. Inactivation of LATS1 by antibody microinjection or RNA-mediated interference in cells, or gene knockout in mice, abrogates cytokinesis and increases the percentage of multinucleate cells. Our findings indicate that LATS1 is a novel cytoskeleton regulator that affects cytokinesis by regulating actin polymerization through negative modulation of LIMK1. [ABSTRACT FROM AUTHOR]

Disrupting mechanisms that control cell proliferation, cell size and apoptosis can cause changes in animal and tissue size and contribute to diseases such as cancer. The LATS family of serine/threonine kinases control tissue size by regulating cell proliferation and function as tumor suppressor genes in both Drosophila and mammals. In order to understand the role of lats in size regulation, we performed a genetic modifier screen in Drosophila to identify components of the lats signaling pathway. Mutations in the Drosophila homolog of C-terminal Src kinase (dcsk) were identified as dominant modifiers of both lats gain-of-function and loss-of-function phenotypes. Homozygous dcsk mutants have enlarged tissue phenotypes similar to lats and FACS and immunohistochemistry analysis of these tissues revealed that dcsk also regulates cell proliferation during development. Animals having mutations in both dcsk and lats display cell overproliferation phenotypes more severe than either mutant alone, demonstrating these genes function together in vivo to regulate cell numbers. Furthermore, homozygous dcsk phenotypes can be partially suppressed by overexpression of lats, indicating that lats is a downstream mediator of dcsk function in vivo. Finally, we show that dCSK phosphorylates LATS in vitro at a conserved C-terminal tyrosine residue, which is critical for normal LATS function in vivo. Taken together, these results demonstrate a role for dCSK in regulating cell numbers during development by inhibiting cell proliferation and suggest that lats is one of the mediators of the dcsk phenotype.Oncogene (2003) 22, 6436-6444. doi:10.1038/sj.onc.1206820 [ABSTRACT FROM AUTHOR]

The lats gene encodes a family of proteins conserved from insects to humans. Drosophila carrying lats mutant cells or mice deficient for Lats1 develop tumors in various tissues. The mammalian LATS1 protein was previously shown to bind to CDC2, suggesting that LATS1 may modulate G2/M cell cycle progression by affecting CDC2 activity. In this study, we introduced human LATS1 into LATS-/- MEF cells by adenovirus-mediated gene transfer. Overexpression of LATS1 causes G2/M arrest through inhibition of CDC2 kinase activity. Furthermore, overexpression of LATS1 significantly suppressed the human tumor cell growth in vitro and tumorigenicity in vivo by inducing either cell cycle arrest in G2/M or apoptosis. These observations suggest that LATS1 is a potent growth suppressor and, like other tumor suppressors, it suppresses growth by inducing cell cycle arrest or apoptosis. Oncogene (2001) 20, 6516–6523. [ABSTRACT FROM AUTHOR]

Multiple signalling events interact in cancer cells. Oncogenic Ras cooperates with Egfr, which cannot be explained by the canonical signalling paradigm. In turn, Egfr cooperates with Hedgehog signalling. How oncogenic Ras elicits and integrates Egfr and Hedgehog signals to drive overgrowth remains unclear. Using a Drosophila tumour model, we show that Egfr cooperates with oncogenic Ras via Arf6, which functions as a novel regulator of Hh signalling. Oncogenic Ras induces the expression of Egfr ligands. Egfr then signals through Arf6, which regulates Hh transport to promote Hh signalling. Blocking any step of this signalling cascade inhibits Hh signalling and correspondingly suppresses the growth of both, fly and human cancer cells harbouring oncogenic Ras mutations. These findings highlight a non-canonical Egfr signalling mechanism, centered on Arf6 as a novel regulator of Hh signalling. This explains both, the puzzling requirement of Egfr in oncogenic Ras-mediated overgrowth and the cooperation between Egfr and Hedgehog. [ABSTRACT FROM AUTHOR]