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Discrete Steps (discrete + step)
Selected AbstractsA robust algorithm for configurational-force-driven brittle crack propagation with R-adaptive mesh alignmentINTERNATIONAL JOURNAL FOR NUMERICAL METHODS IN ENGINEERING, Issue 2 2007C. Miehe Abstract The paper considers a variational formulation of brittle fracture in elastic solids and proposes a numerical implementation by a finite element method. On the theoretical side, we outline a consistent thermodynamic framework for crack propagation in an elastic solid. It is shown that both the elastic equilibrium response as well as the local crack evolution follow in a natural format by exploitation of a global Clausius,Planck inequality in the sense of Coleman's method. Here, the canonical direction of the crack propagation associated with the classical Griffith criterion is the direction of the material configurational force which maximizes the local dissipation at the crack tip and minimizes the incremental energy release. On the numerical side, we exploit this variational structure in terms of crack-driving configurational forces. First, a standard finite element discretization in space yields a discrete formulation of the global dissipation in terms configurational nodal forces. As a consequence, the constitutive setting of crack propagation in the space-discretized finite element context is naturally related to discrete nodes of a typical finite element mesh. Next, consistent with the node-based setting, the discretization of the evolving crack discontinuity is performed by the doubling of critical nodes and interface segments of the mesh. Critical for the success of this procedure is its embedding into an r-adaptive crack-segment reorientation procedure with configurational-force-based directional indicator. Here, successive crack releases appear in discrete steps associated with the given space discretization. These are performed by a staggered loading,release algorithm of energy minimization at frozen crack state followed by the successive crack releases at frozen deformation. This constitutes a sequence of positive-definite discrete subproblems with successively decreasing overall stiffness, providing an extremely robust algorithmic setting in the postcritical range. We demonstrate the performance of the formulation by means of representative numerical simulations. Copyright © 2007 John Wiley & Sons, Ltd. [source] Effect of dexamethasone withdrawal on osteoblastic differentiation of bone marrow stromal cellsJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 1 2003Ryan M. Porter Abstract Dexamethasone is capable of directing osteoblastic differentiation of bone marrow stromal cells (BMSCs) in vitro, but its effects are not lineage-specific, and sustained exposure has been shown to down-regulate collagen synthesis and induce maturation of an adipocyte subpopulation within BMSC cultures. Such side effects might be reduced if dexamethasone is applied in a regimented manner, but the discrete steps in osteoblastic maturation that are stimulated by dexamethasone are not known. To examine this, dexamethasone was added to medium to initiate differentiation of rat BMSCs cultures and then removed after a varying number of days. Cell layers were analyzed for cell number, rate of collagen synthesis, expression of osteocalcin (OC), bone sialoprotein (BSP) and lipoprotein lipase (LpL), and matrix mineralization. Withdrawal of dexamethasone at 3 and 10 days was found to enhance cell number relative to continuous exposure, but did not affect to decrease collagen synthesis slightly. Late markers of osteoblastic differentiation, BSP expression and matrix mineralization, were also sensitive to dexamethasone and increased systematically with exposure while LpL systematically decreased. These results indicate that dexamethasone acts at both early and late stages to direct proliferative osteoprogenitor cells toward terminal maturation. J. Cell. Biochem. 90: 13,22, 2003. © 2003 Wiley-Liss, Inc. [source] Sequential loss of cell cycle checkpoint control contributes to malignant transformation of murine embryonic fibroblasts induced by 20-methylcholanthreneJOURNAL OF CELLULAR PHYSIOLOGY, Issue 1 2010Sudeshna Mukherjee Definitive information about the number and nature of discrete steps of tumorigenesis is enigmatic. To understand the multistep nature of carcinogenesis, an in vitro model of 20-Methylcholanthrene-treated primary fibroblast cells CNCI-PM-20, from 20-day old Swiss mouse embryo was used. Visible neoplastic changes with distinct morphological variations along with specific chromosomal aberrations like Robertsonian metacentrics, double and single-minute chromosomes and aneuploidy were observed from Passage-20 onwards. The cell cycle profile showed gradual increase in G2/M population till P-32, followed by evasion of block from P-36 onwards. Gradual increase in expression of C-myc, CyclinD1 and a decrease in expression of P21 was observed from P-20 onwards. CDC25A expression was significantly increased at P-27 and remained more or less constant in subsequent passages. Additionally, an increased P16 and P53 expression were seen at P-20 followed by their significant down-regulation at P-32. An increased level of phosphorylated retinoblastoma (ppRb) was observed from P-27, probably responsible for a compromised G1/S checkpoint. The inactivation of p21 and p16 might be due to their promoter hyper-methylation as suggested through de-methylation experiment by 5-aza-deoxycytidine at P-42. G2/M checkpoint abrogation was marked by gradual increase in expression of CyclinB1 and Cdc20, and a significant increase of Mad2 at P-20. Interestingly, increased expression of phospho-ATM, ATR and phospho-Chk1 were also seen at P-20 followed by their down-regulation at subsequent passages, indicating a perturbation of DNA damage response pathway at early passages. Our findings therefore dramatize the multiple genetic events that can cooperate to promote tumorigenesis. J. Cell. Physiol. 224:49,58, 2010 © 2010 Wiley-Liss, Inc. [source] Reducing the cost of resistance; experimental evolution in the filamentous fungus Aspergillus nidulansJOURNAL OF EVOLUTIONARY BIOLOGY, Issue 4 2006S. E. SCHOUSTRA Abstract We have studied compensatory evolution in a fludioxonil resistant mutant of the filamentous fungus Aspergillus nidulans. In an evolution experiment lasting for 27 weeks (about 3000 cell cycles) 35 parallel strains of this mutant evolved in three different environmental conditions. Our results show a severe cost of resistance (56%) in the absence of fludioxonil and in all conditions the mutant strain was able to restore fitness without loss of the resistance. In several cases, the evolved strain reached a higher fitness than the original sensitive ancestor. Fitness compensation occurred in one, two or three discrete steps. Genetic analysis of crosses between different evolved strains and between evolved and ancestral strains revealed interaction between compensatory mutations and provided information on the number of loci involved in fitness compensation. In addition, we discuss the opportunities for the experimental study of evolutionary processes provided by the filamentous fungus A. nidulans. [source] A micro-simulation model of firms: Applications of concepts of the demography of the firmPAPERS IN REGIONAL SCIENCE, Issue 2 2000Leo van Wissen Demography of the firm; regional economic growth; micro-simulation; firm formation; firm dissolution Abstract. Recently, there is an increasing demand in spatial planning for models based on the demographic concepts of birth and death of firms. This article describes the structure of a spatial demographic simulation model of firms, and its application within The Netherlands. The model structure is essentially of the familiar demographic cohort component type, where an initial cohort of firms ages in a number of discrete steps, and where in each step additions and subtractions to and from the population are modelled using birth, death and migration components. Apart from the central processes of birth, death and migration, the type of economic activity and firm size are highly important for understanding firm behaviour over time. The article describes the transition functions for each of the demographic components and for firm growth. In addition, some empirical results are presented of a number of model simulations in The Netherlands. The results were partly validated using observed economic demographic data. It is concluded that a substantial amount of work remains to be done in this new field. The model presented here has direct implications for the research agenda of the study of the demography of the firm. [source] | ||||||||||