Hip simulators are designed to reproduce the forces and motion patterns of normal walking. In vivo demands on total hip replacements, however, are varied and often more severe than normal walking conditions. It is these severe conditions that often lead to implant failure. This is clinically based research aimed at understanding some of the more severe conditions in hips and the effect that these have on the performance of the total hip replacement. The polyethylene liner can act as a pump in an acetabular component, forcing fluid and wear particles through the holes to the retroacetabular bone causing osteolysis. Ten patients were studied at revision surgery. Pressures were measured in retroacetabular osteolytic lesions while performing pumping manouvers with the hip. Two laboratory experiments were then designed to study pumping mechanisms in vitro. In patients with contained osteolytic lesions, fluid pressure fluctuations could be measured in the lesion in association with the pumping action. Patients with uncontained osteolytic lesions showed no such pressure fluctuations. In the laboratory we identified 3 distinct mechanisms whereby fluid can be pumped from the hip joint to the retroacetabular bone. These pumping effects could be mitigated by improved implant design. Loading of the femoral head against the edge of the acetabular component produces dramatically increased contact pressures particularly in hard-on-hard bearings. In an analysis of 16 retrieved ceramic-on-ceramic bearings we were able to characterise the mechanism of edge loading based on the pattern of edge loading wear on the bearing surface. Finally in a radiographic study of patients with squeaking ceramic-on-ceramic hips. Squeaking was found to be associated with acetabular component malposition. It seems that edge loading or impingement may be an associated factor in these cases.

Understanding the molecular basis of Mendelian disorders featuring joint dislocation can enhance the knowledge of genetic or cellular pathways required in joint development, and provide candidate genes for studying related complex disorders, such as developmental dysplasia of the hip. Two strategies were employed in this project to investigate Mendelian contributors to congenital joint dislocation. The first strategy was to investigate in-depth a gene known to be associated with joint dislocation. Missense mutations or small in-frame deletions in FLNB, encoding filamin B, have previously been associated with a spectrum of osteochondrodysplasias. Screening a larger cohort established FLNB as the sole underlying disease gene for atelosteogenesis type I and III and also boomerang dysplasia, which was previously thought clinically to be allelic to AOI. Mutations in FLNB cause a large proportion of Larsen syndrome cases with phenotypes reminiscent of the early case series reported. Atypical or "recessive" Larsen syndrome may therefore be due to a different underlying genetic aberration. The disease-associated amino acid substitutions or in-frame deletion/insertions cluster to two main regions of the filamin B protein: the calponin homology 2 domain of the actin-binding domain, and repeats 13-17 of the rod domain. To analyse the functions of these regions, yeast two-hybrid analyses were performed. No interactors were identified with the calponin homology 2 domain, which suggests the amino acid substitutions may disrupt actin binding or the regulation thereof. A candidate interactor, centromere protein J, was identified that binds to repeats 13-15, and could suggest a model for aberrant cell division seen in growth plates of bones of individuals with atelosteogenesis types I and III and boomerang dysplasia. The second strategy used in this project was to investigate the genetic cause of a novel syndrome featuring joint dislocation. A neurocutaneous phenotype segregated in a consanguineous New Zealand family, and through a genetic mapping strategy, a significantly linked locus was identified at 10q23 (Z = 3.63), in which segregation of a common ancestral haplotype fits the linkage hypothesis of homozygosity by descent. Candidate gene analysis and subsequent screening identified a missense mutation 2350C>T in ALDH18A1, which predicts the substitution H784Y in the encoded protein [Delta]�-pyrroline-5-carboxylate synthase (P5CS). The known function of P5CS in proline and ornithine biosynthesis was not affected by the presence of H784Y in an indirect assay, and therefore the hypothesis proposed was that a novel, unknown moonlighting function of P5CS is perturbed causing the phenotype segregating in the family. As an initial exploration of functions of P5CS in the cell, yeast two-hybrid analysis was undertaken. This project examined the contribution of two genes, FLNB and ALDH18A1, to Mendelian congenital joint dislocations. How the cellular functions of the encoded proteins in the cytoskeleton, metabolism, or signal transduction, are critical for joint development is ill understood. Future investigations aimed at identifying candidate genes that confer susceptibility to developmental dysplasia of the hip should consider candidate genes that encode proteins related in function to the products of the FLNB and ALDH18A1 genes.

Habilitation-Thesis--Cologne. / Includes bibliographical references (p. 45-48) and index.

According to the World Health Organisation, hip fracture among elderly people is a global public health problem, with 1.7 million cases worldwide in 1991, a figure due to the aging population and believed likely to increase. Post-operative delirium is a common complication following hip-fracture surgery, and occurs in 25% to 65% of cases (Gustafson 1988). It not only affects the rehabilitation progress of the elderly, but also prolongs hospitalisation, which in turn increases the financial burden on the government. There are different ways of managing post-operative delirium among the elderly, including pharmacological and multifactorial interventions and education programmes. However, there is no standard nursing management of post-operative delirium in Hong Kong, and this affects both patient care and nursing standards. According to the National Institute for Health and Clinical Excellence (2011), multifactorial intervention is cost-effective and an effective method of reducing postoperative delirium, where nurses play an important role as gatekeepers, and thus allow such intervention to be introduced into the clinical setting. With this in mind, translational nursing research was performed by a review of four studies, to introduce the concept of multifactorial intervention to nurses, to formulate the implementation for the intervention, and finally to obtain feedback from colleagues. / published_or_final_version / Nursing Studies / Master / Master of Nursing

No description available.

Femoro-Acetabular Impingement (FAI) is a hip joint disease which affects and impairs the range of hip motion during performing activities of daily living, jogging, walking, or climbing stairs due to the bony abnormalities of the joint. Ballet dancers and athletes (e.g. gymnasts and hockey players) put their hips at the risk of FAI by extremely moving the hip mainly by excessively rotating the joint. In this research, we introduce a visualization system which helps surgeons to analyze the range of hip motions as well as to have a better communication with patients. These goals are achieved by presenting three dimensional (3D) visualizations of motion envelope by examining the maximum possible rotation of the digital hip bones. Our computer simulation system estimates, analyzes and visualizes the maximum hip range of motion (ROM) for the constructed 3D bone models that are extracted from Magnetic Resonance Images (MRI) after segmenting the bones. These tasks are accomplished by first calculating Hip Joint Center (HJC) which is center of rotation of femoral head on the 3D segmented MRI models followed by simulating hip motions with examining impingement between the femur and the acetabulum using our collision detection system. In our collision detection system, surfaces of femoral head and acetabulum bones are sampled in the spherical coordinates based on rasterization and interpolation. Then, the distance between the femoral head and acetabulum are computed to prevent impingement between them. The maximum motion degree of femur bone within depression of acetabulum in every direction during the digital simulation shows the ROMs of the inputted MRI of the hip joint. Six primary plane motions (flexion/extension, abduction/adduction and internal/external rotation) as well as various combinations of these motions (maximum rotation of the hip between every two rotational movements) and successive movements (maximum rotational movement of the hip per another rotational movement) are simulated and analyzed along with 3D visualization of estimated range of these motions. Generally, the ROM differs by some factors such as age, gender, ethnicity, and geographic location. For instance, newborns up to age two have considerably greater motion in hip flexion and hip abduction than adults. Our system by 3D visualization of motion envelope will provide a platform to understand quicker and better the effect of bony morphology of the hip joint on the possible ROM. We also examine the long-standing question about moving center of rotation related to ROM. We found out the ROM becomes bigger especially when the center moves outward to the direction of acetabulum axis. This thesis does not consider the effect of muscle and other surrounding connective tissue on the hip ROM since they can be altered significantly by physical training to show the potential of maximum ROM. For example a ballerina has a bigger ROM leading a bigger motion envelope compared with non-dancers. Hence we visualize the range of joint motions and their envelopes that are obtained from the osseous anatomy of the hip joint. The osseous anatomy of the joint is the most fundamental and permanent factor of ROM which indicates the maximum motion that the joint can achieve if the muscle and other connective tissues are perfectly trained.

Understanding the molecular basis of Mendelian disorders featuring joint dislocation can enhance the knowledge of genetic or cellular pathways required in joint development, and provide candidate genes for studying related complex disorders, such as developmental dysplasia of the hip. Two strategies were employed in this project to investigate Mendelian contributors to congenital joint dislocation. The first strategy was to investigate in-depth a gene known to be associated with joint dislocation. Missense mutations or small in-frame deletions in FLNB, encoding filamin B, have previously been associated with a spectrum of osteochondrodysplasias. Screening a larger cohort established FLNB as the sole underlying disease gene for atelosteogenesis type I and III and also boomerang dysplasia, which was previously thought clinically to be allelic to AOI. Mutations in FLNB cause a large proportion of Larsen syndrome cases with phenotypes reminiscent of the early case series reported. Atypical or "recessive" Larsen syndrome may therefore be due to a different underlying genetic aberration. The disease-associated amino acid substitutions or in-frame deletion/insertions cluster to two main regions of the filamin B protein: the calponin homology 2 domain of the actin-binding domain, and repeats 13-17 of the rod domain. To analyse the functions of these regions, yeast two-hybrid analyses were performed. No interactors were identified with the calponin homology 2 domain, which suggests the amino acid substitutions may disrupt actin binding or the regulation thereof. A candidate interactor, centromere protein J, was identified that binds to repeats 13-15, and could suggest a model for aberrant cell division seen in growth plates of bones of individuals with atelosteogenesis types I and III and boomerang dysplasia. The second strategy used in this project was to investigate the genetic cause of a novel syndrome featuring joint dislocation. A neurocutaneous phenotype segregated in a consanguineous New Zealand family, and through a genetic mapping strategy, a significantly linked locus was identified at 10q23 (Z = 3.63), in which segregation of a common ancestral haplotype fits the linkage hypothesis of homozygosity by descent. Candidate gene analysis and subsequent screening identified a missense mutation 2350C>T in ALDH18A1, which predicts the substitution H784Y in the encoded protein [Delta]�-pyrroline-5-carboxylate synthase (P5CS). The known function of P5CS in proline and ornithine biosynthesis was not affected by the presence of H784Y in an indirect assay, and therefore the hypothesis proposed was that a novel, unknown moonlighting function of P5CS is perturbed causing the phenotype segregating in the family. As an initial exploration of functions of P5CS in the cell, yeast two-hybrid analysis was undertaken. This project examined the contribution of two genes, FLNB and ALDH18A1, to Mendelian congenital joint dislocations. How the cellular functions of the encoded proteins in the cytoskeleton, metabolism, or signal transduction, are critical for joint development is ill understood. Future investigations aimed at identifying candidate genes that confer susceptibility to developmental dysplasia of the hip should consider candidate genes that encode proteins related in function to the products of the FLNB and ALDH18A1 genes.

Thesis (MAppSc in Physiotherapy)--University of South Australia, 1997

Thesis (MHlthSc(OccTh))--University of South Australia, 1999

Thesis (MAppSc in Physiotherapy) -- University of South Australia, 1992