Modelling Deformations in Car Crash animation

In this paper, we present a prototype of a deformation engine to efficiently model and render the damaged structure of vehicles in crash scenarios. We introduce a novel system architecture to accelerate the computation, which is traditionally an extremely expensive task. We alter a rigid body simulator to predict trajectories of cars during a collision and formulate a correction procedure to estimate the deformations of the collapsed car structures within the contact area. Non-linear deformations are solved based on the principle of energy conservation. Large plastic deformations resulting from collisions are modelled as a weighted combination of deformation examples of beams which can be produced using classical mechanics

Slowed muscle oxygen uptake kinetics with raised metabolism are not dependent on blood flow or recruitment dynamics

Oxygen uptake kinetics (τ[Image: see text]) are slowed when exercise is initiated from a raised metabolic rate. Whether this reflects the recruitment of muscle fibres differing in oxidative capacity, or slowed blood flow ([Image: see text]) kinetics is unclear. This study determined τ[Image: see text] in canine muscle in situ, with experimental control over muscle activation and [Image: see text] during contractions initiated from rest and a raised metabolic rate. The gastrocnemius complex of nine anaesthetised, ventilated dogs was isolated and attached to a force transducer. Isometric tetanic contractions (50 Hz; 200 ms duration) via supramaximal sciatic nerve stimulation were used to manipulate metabolic rate: 3 min stimulation at 0.33 Hz (S1), followed by 3 min at 0.67 Hz (S2). Circulation was initially intact (SPON), and subsequently isolated for pump-perfusion (PUMP) above the greatest value in SPON. Muscle [Image: see text] was determined contraction-by-contraction using an ultrasonic flowmeter and venous oximeter, and normalised to tension-time integral (TTI). τ[Image: see text]/TTI and τ[Image: see text] were less in S1(SPON) (mean ± s.d.: 13 ± 3 s and 12 ± 4 s, respectively) than in S2(SPON) (29 ± 19 s and 31 ± 13 s, respectively; P < 0.05). τ[Image: see text]/TTI was unchanged by pump-perfusion (S1(PUMP), 12 ± 4 s; S2(PUMP), 24 ± 6 s; P < 0.001) despite increased O(2) delivery; at S2 onset, venous O(2) saturation was 21 ± 4% and 65 ± 5% in SPON and PUMP, respectively. [Image: see text] kinetics remained slowed when contractions were initiated from a raised metabolic rate despite uniform muscle stimulation and increased O(2) delivery. The intracellular mechanism may relate to a falling energy state, approaching saturating ADP concentration, and/or slowed mitochondrial activation; but further study is required. These data add to the evidence that muscle [Image: see text] control is more complex than previously suggested