Requirements capture for medical device design

Thesis submitted for a M.Phil. degreeSIGLEAvailable from British Library Document Supply Centre-DSC:99/38696 / BLDSC - British Library Document Supply CentreGBUnited Kingdo

Segmenting Mechanomyography Measures of Muscle Activity Phases Using Inertial Data

This dataset contains the data used in our manuscript titled &quot;Segmenting Mechanomyography Measures of Muscle Activity Phases Using Inertial Data&quot;. Data structure is explained in the README.txt file located at the top-level of the dataset. Manuscript title in the README.txt file and contained in the title of the zip file are of a previous working title. Please contact corresponding author Richard B. Woodward for any questions. </span

Structure-mechanics relationships of collagen fibrils in the osteogenesis imperfect mouse model

The collagen molecule, which is the building block of collagen fibrils, is a triple helix of two ?1(I) chains and one ?2(I) chain. However, in the severe mouse model of osteogenesis imperfecta (OIM), deletion of the COL1A2 gene results in the substitution of the ?2(I) chain by one ?1(I) chain. As this substitution severely impairs the structure and mechanics of collagen-rich tissues at the tissue and organ level, the main aim of this study was to investigate how the structure and mechanics are altered in OIM collagen fibrils. Comparing results from atomic force microscopy imaging and cantilever-based nanoindentation on collagen fibrils from OIM and wild-type (WT) animals, we found a 33% lower indentation modulus in OIM when air-dried (bound water present) and an almost fivefold higher indentation modulus in OIM collagen fibrils when fully hydrated (bound and unbound water present) in phosphate-buffered saline solution (PBS) compared with WT collagen fibrils. These mechanical changes were accompanied by an impaired swelling upon hydration within PBS. Our experimental and atomistic simulation results show how the structure and mechanics are altered at the individual collagen fibril level as a result of collagen gene mutation in OIM. We envisage that the combination of experimental and modelling approaches could allow mechanical phenotyping at the collagen fibril level of virtually any alteration of collagen structure or chemistry

Segmenting Phases of Muscle Activity in Pervasive Environments using Mechanomyography and Inertial Measurement Units

<p>This dataset contains the data used in our manuscript titled "Segmenting Phases of Muscle Activity in Pervasive Environments using Mechanomyography and Inertial Measurement Units". Data structure is explained in the README.txt file located at the top-level of the dataset.</p> <p>Please contact corresponding author Richard B. Woodward for any questions.</p

Spontaneous osteoarthritis in Str/ort mice is unlikely due to greater vulnerability to mechanical trauma

SummaryObjectiveRelative contributions of genetic and mechanical factors to osteoarthritis (OA) remain ill-defined. We have used a joint loading model found to produce focal articular cartilage (AC) lesions, to address whether genetic susceptibility to OA in Str/ort mice is related to AC vulnerability to mechanical trauma and whether joint loading influences spontaneous OA development. We also develop finite element (FE) models to examine whether AC thickness may explain any differential vulnerability to load-induced lesions.MethodsRight knees of 8-week-old Str/ort mice were loaded, AC integrity scored and thickness compared to CBA mice. Mechanical forces engendered in this model and the impact of AC thickness were simulated in C57Bl/6 mice using quasi-static FE modelling.ResultsUnlike joints in non-OA prone CBA mice, Str/ort knees did not exhibit lateral femur (LF) lesions in response to applied loading; but exhibited thicker AC. FE modeling showed increased contact pressure and shear on the lateral femoral surface in loaded joints, and these diminished in joints containing thicker AC. Histological analysis of natural lesions in the tibia of Str/ort joints revealed that applied loading increased OA severity, proteoglycan loss and collagen type II degradation.ConclusionGenetic OA susceptibility in Str/ort mice is not apparently related to greater AC vulnerability to trauma, but joint loading modifies severity of natural OA lesions in the medial tibia. FE modelling suggests that thicker AC in Str/ort mice diminishes tissue stresses and protects against load-induced AC lesions in the LF but that this is unrelated to their genetic susceptibility to OA