374 resultados para growth dynamics


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Competitive sailing is characterised by continuous interdependencies of decisions and actions. All actions imply a permanent monitoring of the environmental conditions, such as intensity and direction of the wind, sea characteristics, and the behaviour of the opponent sailors. These constraints on sailors’ behavior are in constant change implying continuous adjustments in sailors’ actions and decisions. Among the different parts of a regatta, tactics and strategy at the start are particularly relevant. Among coaches there is an adage that says that “the start is 50% of a regatta” (Houghton, 1984; Saltonstall, 1983/1986). Olympic sailing regattas are performed with boats of the same class, by one, two or three sailors, depending on the boat class. Normally before the start, sailors visit the racing venue and analyse wind and sea characteristics, in order to fine- tune their boats accordingly. Then, five minutes before the start, sailors initiate starting procedures in order to be in a favourable position at the starting line (at the “second zero”). This position is selected during the start period according to wind shifts tendencies and the actions of other boats (Figure 11.1). Only after the start signal can the boats cross the imaginary starting line between the race committee signal boat “A” and the pin end boat. The start takes place against the wind (upwind), and the boats start racing in the direction of mark 1. Based on the evaluation of the sea and wind characteristics (e.g. if the wind is stronger at a particular place on the course), sailors re- adjust their strategy for the regatta. This strategy may change during the regatta, according to wind changes and adversary actions. More to the point, strategic decisions constrain and are constrained by on- line decisions during the regatta.

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This project was a step forward in the examination and identification of key variables on the perception, decision making and action of team sport athletes through theoretical insights provided by the ecological dynamics perspective. The methodology drew on experiential knowledge of elite coaches to drive further empirical investigation into the specific task, environmental and personal constraints that shape the behaviour of athletes in specific performance contexts. The thesis has provided an effective rationale for further investigation into the emergent perception, decision making and action demanded of athletes in these unpredictable, fluent, fast-paced environments.

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It is well known that track defects cause profound effects to the dynamics of railway wagons; normally such problems are examined for cases of wagons running at a constant speed. Brake/traction torques affect the speed profile due to the wheel–rail contact characteristics but most of the wagon–track interaction models do not explicitly consider them in simulation. The authors have recently published a model for the dynamics of wagons subject to braking traction torques on a perfect track by explicitly considering the pitch degree of freedom for wheelsets. The model is extended for cases of lateral and vertical track geometry defects and worn railhead and wheel profiles. This paper presents the results of the analyses carried out using the model extended to the dynamics of wagons containing less ideal wheel profiles running on tracks with geometry defects and worn rails.

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Understanding the complex mechanisms underlying bone remodeling is crucial to the development of novel therapeutics. Glycosaminoglycans (GAGs) localised to the extracellular matrix (ECM) of bone are thought to play a key role in mediating aspects of bone development. The influence of isolated GAGs was studied by utilising in vitro murine calvarial monolayer and organ culture model systems. Addition of GAG preparations extracted from the cell surface of human osteoblasts at high concentrations (5 microg/ml) resulted in decreased proliferation of cells and decreased suture width and number of bone lining cells in calvarial sections. When we investigated potential interactions between the growth factors fibroblast growth factor-2 (FGF2), bone morphogenic protein-2 (BMP2) and transforming growth factor-beta1 (TGFbeta1) and the isolated cell surface GAGs, differences between the two model systems emerged. The cell culture system demonstrated a potentiating role for the isolated GAGs in the inhibition of FGF2 and TGFbeta1 actions. In contrast, the organ culture system demonstrated an enhanced stimulation of TFGbeta1 effects. These results emphasise the role of the ECM in mediating the interactions between GAGs and growth factors during bone development and suggest the GAG preparations contain potent inhibitory or stimulatory components able to mediate growth factor activity.

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We consider growth and welfare effects of lifetime-uncertainty in an economy with human capital-led endogenous growth. We argue that lifetime uncertainty reduces private incentives to invest in both physical and human capital. Using an overlapping generations framework with finite-lived households we analyze the relevance of government expenditure on health and education to counter such growth-reducing forces. We focus on three different models that differ with respect to the mode of financing of education: (i) both private and public spending, (ii) only public spending, and (iii) only private spending. Results show that models (i) and (iii) outperform model (ii) with respect to long-term growth rates of per capita income, welfare levels and other important macroeconomic indicators. Theoretical predictions of model rankings for these macroeconomic indicators are also supported by observed stylized facts.

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BACKGROUND Endometriosis is a polygenic disease with a complex and multifactorial aetiology that affects 8-10% of women of reproductive age. Epidemiological data support a link between endometriosis and cancers of the reproductive tract. Fibroblast growth factor receptor 2 (FGFR2) has recently been implicated in both endometrial and breast cancer. Our previous studies on endometriosis identified significant linkage to a novel susceptibility locus on chromosome 10q26 and the FGFR2 gene maps within this linkage region. We therefore hypothesized that variation in FGFR2 may contribute to the risk of endometriosis. METHODS We genotyped 13 single nucleotide polymorphisms (SNPs) densely covering a 27 kb region within intron 2 of FGFR2 including two SNPs (rs2981582 and rs1219648) significantly associated with breast cancer and a total 40 tagSNPs across 150 kb of the FGFR2 gene. SNPs were genotyped in 958 endometriosis cases and 959 unrelated controls. RESULTS We found no evidence for association between endometriosis and FGFR2 intron 2 SNPs or SNP haplotypes and no evidence for association between endometriosis and variation across the FGFR2 gene. CONCLUSIONS Common variation in the breast-cancer implicated intron 2 and other highly plausible causative candidate regions of FGFR2 do not appear to be a major contributor to endometriosis susceptibility in our large Australian sample.