Nanotextured surfaces (NTSs) are critical to organisms as self-adaptation and survival tools. These NTSs have been actively mimicked in the process of developing bactericidal surfaces for diverse biomedical and hygiene applications. To design and fabricate bactericidal topographies effectively for various applications, understanding the bactericidal mechanism of NTS in nature is essential. The current mechanistic explanations on natural bactericidal activity of nanopillars have not utilized recent advances in microscopy to study the natural interaction. This research reveals the natural bactericidal interaction between E. coli and a dragonfly wing's (Orthetrum villosovittatum) NTS using advanced microscopy techniques and proposes a model. Contrary to the existing mechanistic models, this experimental approach demonstrated that the NTS of Orthetrum villosovittatum dragonfly wings has two prominent nanopillar populations and the resolved interface shows membrane damage occurred without direct contact of the bacterial cell membrane with the nanopillars. We propose that the bacterial membrane damage is initiated by a combination of strong adhesion between nanopillars and bacterium EPS layer as well as shear force when immobilized bacterium attempts to move on the NTS. These findings could help guide the design of novel biomimetic nanomaterials by maximizing the synergies between biochemical and mechanical bactericidal effects.
Experiments were carried out to investigate the influence of loading velocity on the stiffness of the articular cartilage matrix. Compression tests were conducted on cartilage alone and cartilage-on-bone at strain-rates ranging from 10(-5)sec-1 to 10(3)sec-1 and it was established that matrix stiffness increased progressively in the "low" and "medium" strain-rate regimens and assumes a limiting value at "high" rates of loading up to impact. Analysis of the strain field characteristics associated with the compression process, both at low and high velocities, suggests that two fundamentally different mechanisms of deformation control the development of cartilage matrix stiffness. At low strain-rates a consolidation-dependent stiffness occurs while at high strain rates the high stiffness results from a classical elastic deformation process. This bifurcation in the tissue's response to loading is likely to affect the redistribution of joint contact stresses being transmitted into the subchondral bone.
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