1985 model 172p v speeds
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The transition between gliding and flapping also can be easily explained by the vortex theory.
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This strongly supports the arboreal theory of the evolution of flight in birds, bats, and pterosaurs, which includes a gliding stage before powered flight originated. Any such thrust can be used to make the flight path shallower than it is in equilibrium gliding for the same animal. The outcome is that, given certain flight variables, a net thrust will always be generated during partially powered flight. Given this constraint, the model then explores whether there is any net horizontal thrust beyond that needed to balance body drag. The model is constructed so that the various flight variables always combine in such a way that the vertical lift force produced during one complete wing stroke in partially powered flight by a hypothetical animal always equals the weight of the animal. My model, based on quasi-stationary aerodynamics, shows that sufficient lift and a net thrust can be produced even during very slight flapping in a gliding animal. The criticism is mostly unfounded and lacks adequate explanations. It has been stated, for instance, that incipient flapping during gliding would dramatically reduce lift, and that the generation of vortex rings by wing strokes must be a principal problem for animals to solve in evolving powered flight. The low precision of the estimates from the model (coefficients of variation: 31% for insulin resistance and 32% for beta-cell deficit) limits its use, but the correlation of the model's estimates with patient data accords with the hypothesis that basal glucose and insulin interactions are largely determined by a simple feed back loop.I counter recent criticism against the arboreal theory of the evolution of flight in vertebrates. The estimate of deficient beta-cell function obtained by homeostasis model assessment correlated with that derived using the hyperglycaemic clamp (Rs = 0.61, p less than 0.01) and with the estimate from the intravenous glucose tolerance test (Rs = 0.64, p less than 0.05). There was no correlation with any aspect of insulin-receptor binding. The estimate of insulin resistance obtained by homeostasis model assessment correlated with estimates obtained by use of the euglycaemic clamp (Rs = 0.88, p less than 0.0001), the fasting insulin concentration (Rs = 0.81, p less than 0.0001), and the hyperglycaemic clamp, (Rs = 0.69, p less than 0.01).
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The accuracy and precision of the estimate have been determined by comparison with independent measures of insulin resistance and beta-cell function using hyperglycaemic and euglycaemic clamps and an intravenous glucose tolerance test. Comparison of a patient's fasting values with the model's predictions allows a quantitative assessment of the contributions of insulin resistance and deficient beta-cell function to the fasting hyperglycaemia (homeostasis model assessment, HOMA). A computer-solved model has been used to predict the homeostatic concentrations which arise from varying degrees beta-cell deficiency and insulin resistance. The steady-state basal plasma glucose and insulin concentrations are determined by their interaction in a feedback loop.