The formation of plaques is one of the main causes for the blockage of arteries. This can lead to ischaemic brain or myocardial infarctions as well as other cardiovascular diseases. Possible biochemical and biomechanical processes contribute to the development of plaque growth and rupture. The main biochemical processes are the penetration of monocytes and the accumulation of foam cells in the vessel wall, leading to the formation and growth of plaques. The biomechanical forces can be measured by observing stresses in the blood flow and the vessel wall, which may lead to the rupture of plaques.In this thesis, we formulate an appropriate model to describe the evolution of plaques. The model consists of both the interaction between the blood flow and the vessel wall, and the growth of plaques due to the penetration of monocytes from the blood flow into the vessel wall. The Navier-Stokes equations and the elastic structure equations are used to describe the dynamics of fluid (blood flow) and the mechanics of structure (vessel wall). The motion of monocytes is described by the convection-diffusion-reaction equation, coupled with an equation for the accumulation of foam cells. Finally the metric of growth is introduced to accurately determine the stress tensor, and its evolution equation is derived. The variational formulation of the model is transformed into the ALE (Arbitrary Lagrangian-Eulerian) formulation, and all the equations are rewritten in the fixed domain. Temporal discretization is achieved with finite differences and spatial discretization is based on the Galerkin finite element method. The nonlinear systems are linearized and solved by the Newton method.Based on the model and the numerical methods above, numerical simulations are performed by using the software Gascoigne. The obtained numerical results make an agreement with the observation, and support the assumption that the penetration of monocytes and the accumulation of foam cells lead to the formation and growth of plaques, and that the evolution of plaques induces the increase of stresses in the vessel wall, which is an indicator of plaque rupture. Zusammenfassung

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The results suggest that both clonal expansion and horizontal transmission of IncHI2-type plasmids containing oqxAB and aac(6')-Ib-cr may be involved in the spread of oqxAB in Salmonella Typhimurium isolates in food-producing animals in China. There is a great need to monitor the potential dissemination of this multiresistance gene.

Residue depletion of marbofloxacin in broiler chicken after oral administration at 5 mg/kg/day for three consecutive days was studied in this study. The areas under the concentration-time curve from 0 h to ∞ (AUC0-∞ s) of marbofloxacin in tissues and plasma were used to calculate tissue/plasma partition coefficients (PX s). Based on PX s and the other parameters derived from published studies, a flow-limited physiologically based pharmacokinetics (PBPK) model was developed to predict marbofloxacin concentrations, which were then compared with those derived from the residue depletion study so as to validate this model. Considering individual difference in drug disposition, a Monte Carlo simulation included 1000 iterations was further incorporated into the validated model to generate a population PBPK model and to estimate the marbofloxacin residue withdrawal times in edible tissues. The withdrawal periods were compared to those derived from linear regression analysis. The PBPK model presented here successfully predicted the measured concentrations in all tissues. The withdrawal times in all edible tissues derived from the population PBPK model were longer than those from linear regression analysis, and based on the residues in kidney, a withdrawal time of 4 days was estimated for marbofloxacin after oral administration at 5 mg/kg/day for three consecutive days. It was shown that population PBPK model could be used to accurately predict marbofloxacin residue withdrawal time in edible tissues in broiler chickens.

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