Friction-induced vibration: Model development and comparison with large-scale experimental tests

This paper presents a comparison between theoretical predictions and experimental results from a pin-on-disc test rig exploring friction-induced vibration. The model is based on a linear stability analysis of two systems coupled by sliding contact at a single point. Predictions are compared with a large volume of measured squeal initiations that have been post-processed to extract growth rates and frequencies at the onset of squeal. Initial tests reveal the importance of including both finite contact stiffness and a velocity-dependent dynamic model for friction, giving predictions that accounted for nearly all major clusters of squeal initiations from 0 to 5 kHz. However, a large number of initiations occurred at disc mode frequencies that were not predicted with the same parameters. These frequencies proved remarkably difficult to destabilise, requiring an implausibly high coefficient of friction. An attempt has been made to estimate the dynamic friction behaviour directly from the squeal initiation data, revealing complex-valued frequency-dependent parameters for a new model of linearised dynamic friction. These new parameters readily destabilised the disc modes and provided a consistent model that could account for virtually all initiations from 0 to 15 kHz. The results suggest that instability thresholds for a wide range of squeal-type behaviour can be predicted, but they highlight the central importance of a correct understanding and accurate description of dynamic friction at the sliding interface. © 2013 Elsevier Ltd. All rights reserved.

Bacterial growth rate and host factors as determinants of intracellular bacterial distributions in systemic Salmonella enterica infections.

Bacteria of the species Salmonella enterica cause a range of life-threatening diseases in humans and animals worldwide. The within-host quantitative, spatial, and temporal dynamics of S. enterica interactions are key to understanding how immunity acts on these infections and how bacteria evade immune surveillance. In this study, we test hypotheses generated from mathematical models of in vivo dynamics of Salmonella infections with experimental observation of bacteria at the single-cell level in infected mouse organs to improve our understanding of the dynamic interactions between host and bacterial mechanisms that determine net growth rates of S. enterica within the host. We show that both bacterial and host factors determine the numerical distributions of bacteria within host cells and thus the level of dispersiveness of the infection.