Populations are aging and the prevalence of chronic disease, persisting for many years, is increasing. The most common, non-communicable chronic diseases in developed countries are; cardiovascular disease (CVD), type 2 diabetes, obesity, arthritis and specific cancers. Chronic diseases such as cardiovascular disease, type 2 diabetes and obesity have high prevalence and develop over the course of life due to a number of interrelated factors including genetic predisposition, nutrition and lifestyle. With the development and completion of human genome sequencing, we are able to trace genes responsible for proteins and metabolites that are linked with these diseases. A computerized model focused on organizing knowledge related to genes, nutrition and the three chronic diseases, namely, cardiovascular disease, type 2 diabetes and obesity has been developed for the Ontology-Based Personalized Risk Evaluation for Chronic Disease Project. This model is a Protégé-based ontological representation which has been developed for entering and linking concepts and data for these three chronic diseases. This model facilitates to identify interrelationships between concepts. The ontological representation provides the framework into which information on individual patients, disease symptoms, gene maps, diet and life history can be input, and risks, profiles, and recommendations derived. Personal genome and health data could provide a guide for designing and building a medical health administration system for taking relevant annual medical tests, e.g. gene expression level changes for health surveillance. One method, called transductive neuro-fuzzy inference system with weighted data normalization is used to evaluate personalized risk of chronic disease. This personalized approach has been used for two different chronic diseases, predicting the risk of cardiovascular disease and predicting the risk of type 2 diabetes. For predicting the risk of cardiovascular disease, the National Nutrition Health Survey 97 data from New Zealand population has been used. This data contains clinical, anthropometric and nutritional variables. For predicting risk of type 2 diabetes, data from the Italian population with clinical and genetic variables has been used. It has been discovered that genes responsible for causing type 2 diabetes are different in male and female samples. A framework to integrate the personalized model and the chronic disease ontology is also developed with the aim of providing support for further discovery through the integration of the ontological representation in order to build an expert system in genes of interest and relevant dietary components.

Populations are aging and the prevalence of chronic disease, persisting for many years, is increasing. The most common, non-communicable chronic diseases in developed countries are; cardiovascular disease (CVD), type 2 diabetes, obesity, arthritis and specific cancers. Chronic diseases such as cardiovascular disease, type 2 diabetes and obesity have high prevalence and develop over the course of life due to a number of interrelated factors including genetic predisposition, nutrition and lifestyle. With the development and completion of human genome sequencing, we are able to trace genes responsible for proteins and metabolites that are linked with these diseases. A computerized model focused on organizing knowledge related to genes, nutrition and the three chronic diseases, namely, cardiovascular disease, type 2 diabetes and obesity has been developed for the Ontology-Based Personalized Risk Evaluation for Chronic Disease Project. This model is a Protégé-based ontological representation which has been developed for entering and linking concepts and data for these three chronic diseases. This model facilitates to identify interrelationships between concepts. The ontological representation provides the framework into which information on individual patients, disease symptoms, gene maps, diet and life history can be input, and risks, profiles, and recommendations derived. Personal genome and health data could provide a guide for designing and building a medical health administration system for taking relevant annual medical tests, e.g. gene expression level changes for health surveillance. One method, called transductive neuro-fuzzy inference system with weighted data normalization is used to evaluate personalized risk of chronic disease. This personalized approach has been used for two different chronic diseases, predicting the risk of cardiovascular disease and predicting the risk of type 2 diabetes. For predicting the risk of cardiovascular disease, the National Nutrition Health Survey 97 data from New Zealand population has been used. This data contains clinical, anthropometric and nutritional variables. For predicting risk of type 2 diabetes, data from the Italian population with clinical and genetic variables has been used. It has been discovered that genes responsible for causing type 2 diabetes are different in male and female samples. A framework to integrate the personalized model and the chronic disease ontology is also developed with the aim of providing support for further discovery through the integration of the ontological representation in order to build an expert system in genes of interest and relevant dietary components.

Introduction Bacterial biofilms have been implicated in the pathogenesis of Chronic Rhinosinusitis (CRS). This thesis consists of a number of separate studies. The results of each study were designed to help provide an evolution of knowledge that could be applied to our subsequent investigations on the topic of bacterial biofilms and chronic rhinosinusitis. In vitro studies were utilized to document the capacity of CRS bacteria to form biofilms as well as to investigate the efficacy of various antimicrobials at high concentrations. Additionally, an in vivo sheep model was developed to examine different biofilm detection techniques. Finally, a study of CRS patients was conducted to investigate the incidence of biofilm related sinus disease. Methods Our in vitro studies used 96 well crystal violet microtiter plate assays to determine the biofilm growth characteristics of S.aureus isolated from patients with CRS. Established biofilms were then subjected various antimicrobial agents, and the degree of biofilm reduction calculated to examine their potential for sinus biofilm treatment. A sheep sinusitis model involved performing endoscopic sinus surgery, occlusion of frontal sinus ostia and the introduction of bacteria. Mucosal specimens were subsequently examined for the presence of bacterial biofilms using transmission electron microscopy (TEM), scanning electron microscopy (SEM) and confocal scanning laser microscopy (CSLM). CSLM was also used in a prospective study to document the presence bacterial biofilms on the mucosa of patients with CRS compared to controls. Results The findings of in vitro experiments revealed that not all isolates were capable of forming biofilms. Of the antibiotics tested, only Mupirocin was capable of reducing biofilm mass by 90% in all isolates. The animal model showed considerable variation in biofilm detection rates. The CSLM biofilm detection rate was 100% in obstructed sinuses with bacteria introduced, whereas TEM detected only 66%. Both these objective measures failed to identify biofilms in control groups. SEM found biofilms in all experimental groups including controls. CSLM analysis of CRS patients found Bacterial biofilms in 44% and no biofilms in controls. Conclusion The demonstration of biofilms in the sheep model for sinusitis and biofilms on the mucosal specimens of patients with CRS, and the ability of bacteria in CRS to form biofilms in vitro, further supports the hypothesis that biofilms play a role in the pathogenesis of CRS. CSLM is the modality of choice in documenting the presence of bacterial biofilms on sinus mucosal surfaces due to the inherent flaws of sampling error and subjectivity of TEM and SEM. Finally, CRS is a multi-factorial disease, topical Mupirocin via nasal irrigation may be a therapeutic option in patients with likely S.aureus biofilms. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1367183 / Thesis (M.S.) - University of Adelaide, School of Medicine, 2009

Populations are aging and the prevalence of chronic disease, persisting for many years, is increasing. The most common, non-communicable chronic diseases in developed countries are; cardiovascular disease (CVD), type 2 diabetes, obesity, arthritis and specific cancers. Chronic diseases such as cardiovascular disease, type 2 diabetes and obesity have high prevalence and develop over the course of life due to a number of interrelated factors including genetic predisposition, nutrition and lifestyle. With the development and completion of human genome sequencing, we are able to trace genes responsible for proteins and metabolites that are linked with these diseases. A computerized model focused on organizing knowledge related to genes, nutrition and the three chronic diseases, namely, cardiovascular disease, type 2 diabetes and obesity has been developed for the Ontology-Based Personalized Risk Evaluation for Chronic Disease Project. This model is a Protégé-based ontological representation which has been developed for entering and linking concepts and data for these three chronic diseases. This model facilitates to identify interrelationships between concepts. The ontological representation provides the framework into which information on individual patients, disease symptoms, gene maps, diet and life history can be input, and risks, profiles, and recommendations derived. Personal genome and health data could provide a guide for designing and building a medical health administration system for taking relevant annual medical tests, e.g. gene expression level changes for health surveillance. One method, called transductive neuro-fuzzy inference system with weighted data normalization is used to evaluate personalized risk of chronic disease. This personalized approach has been used for two different chronic diseases, predicting the risk of cardiovascular disease and predicting the risk of type 2 diabetes. For predicting the risk of cardiovascular disease, the National Nutrition Health Survey 97 data from New Zealand population has been used. This data contains clinical, anthropometric and nutritional variables. For predicting risk of type 2 diabetes, data from the Italian population with clinical and genetic variables has been used. It has been discovered that genes responsible for causing type 2 diabetes are different in male and female samples. A framework to integrate the personalized model and the chronic disease ontology is also developed with the aim of providing support for further discovery through the integration of the ontological representation in order to build an expert system in genes of interest and relevant dietary components.

Introduction Bacterial biofilms have been implicated in the pathogenesis of Chronic Rhinosinusitis (CRS). This thesis consists of a number of separate studies. The results of each study were designed to help provide an evolution of knowledge that could be applied to our subsequent investigations on the topic of bacterial biofilms and chronic rhinosinusitis. In vitro studies were utilized to document the capacity of CRS bacteria to form biofilms as well as to investigate the efficacy of various antimicrobials at high concentrations. Additionally, an in vivo sheep model was developed to examine different biofilm detection techniques. Finally, a study of CRS patients was conducted to investigate the incidence of biofilm related sinus disease. Methods Our in vitro studies used 96 well crystal violet microtiter plate assays to determine the biofilm growth characteristics of S.aureus isolated from patients with CRS. Established biofilms were then subjected various antimicrobial agents, and the degree of biofilm reduction calculated to examine their potential for sinus biofilm treatment. A sheep sinusitis model involved performing endoscopic sinus surgery, occlusion of frontal sinus ostia and the introduction of bacteria. Mucosal specimens were subsequently examined for the presence of bacterial biofilms using transmission electron microscopy (TEM), scanning electron microscopy (SEM) and confocal scanning laser microscopy (CSLM). CSLM was also used in a prospective study to document the presence bacterial biofilms on the mucosa of patients with CRS compared to controls. Results The findings of in vitro experiments revealed that not all isolates were capable of forming biofilms. Of the antibiotics tested, only Mupirocin was capable of reducing biofilm mass by 90% in all isolates. The animal model showed considerable variation in biofilm detection rates. The CSLM biofilm detection rate was 100% in obstructed sinuses with bacteria introduced, whereas TEM detected only 66%. Both these objective measures failed to identify biofilms in control groups. SEM found biofilms in all experimental groups including controls. CSLM analysis of CRS patients found Bacterial biofilms in 44% and no biofilms in controls. Conclusion The demonstration of biofilms in the sheep model for sinusitis and biofilms on the mucosal specimens of patients with CRS, and the ability of bacteria in CRS to form biofilms in vitro, further supports the hypothesis that biofilms play a role in the pathogenesis of CRS. CSLM is the modality of choice in documenting the presence of bacterial biofilms on sinus mucosal surfaces due to the inherent flaws of sampling error and subjectivity of TEM and SEM. Finally, CRS is a multi-factorial disease, topical Mupirocin via nasal irrigation may be a therapeutic option in patients with likely S.aureus biofilms. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1367183 / Thesis (M.S.) - University of Adelaide, School of Medicine, 2009

Cognitive-behavioural based models of chronic pain contend that appraisals of harm affect the individual�s response to pain. It has been suggested that fear of pain and/or anxiety sensitivity predispose individuals to chronicity. However, other factors such as pain self-efficacy are believed to mediate between experience of pain and disability. According to this view, pain is maintained through hypervigilance towards painful sensations and subsequent avoidance. Four studies were conducted in order to evaluate the structure of fear-avoidance models of chronic pain, and also, to examine the role of hypervigilance as an underlying mechanism in maintenance of pain. In study one, using a sample of 207 consecutive patients, two models were tested. First, fear of movement model as proposed by Vlaeyen et al. (1995a) was examined. It was found that negative affectivity has direct effects on the fear and avoidance of pain, which in turn, contributes to disability. In total, fear/avoidance accounted for a significant amount of the variance of disability. In addition, severity of pain was found to increase pain disability, while itself is influenced still by negative affectivity. These findings supported the model of fear of pain as described by Vlaeyen et al. (1995a). Further, we found that self-efficacy may mediate the impact of fear of pain on disability and reduces the perceived physical disability. At the same time, self-efficacy was shown to have direct reductive impact on disability. However, both studies indicated that people who are fearful in response to pain are more likely to develop disability, although self-efficacy may play a moderating role. In the studies one, two, and three, the role of hypervigilance in over attending to pain was investigated. In study one a large sample of 168 chronic pain patients were studied. Questionnaires measuring different aspects of pain and a computerised version of the Dot-Probe Task were administered. Four types of words related to different dimensions of pain and matched neutral words were used as stimuli. Reaction times in response to the stimuli were recorded. A factorial design 3x4x2x2 and ANOVAs were employed to analyse the data. Chronic pain patients showed a cognitive bias to sensory pain words relative to affective, disability, and threat-related words. However, contrary to expectations, those high in fear of pain responded more slowly to stimuli than those less fearful of pain. These results suggest that patients with chronic pain problems selectively attend to sensory aspects of pain. However, selective attention appears to depend upon the nature of pain stimuli. For those who are highly fearful of pain they may not only selectively attend to pain-related information but also have difficulty disengaging from those stimuli. In study two, 35 chronic pain patients were compared with the same number matched healthy subjects. Both groups completed measures of fear of pain, anxiety sensitivity, depression and anxiety, in addition to dot probe task. Results indicated that both groups show similar attentional bias to sensory words in comparison with other word types. However, the level of this biasness was higher for chronic pain patients. Lack of significant differences between patients and controls is discussed in the context of possible evolutionary value of sensitivity to pain as an adaptive reaction in healthy controls, and contrary, as a maladaptive response to pain in chronic pain patients. The results of the previous research suggest that chronic pain patients demonstrate cognitive biases towards pain-related information and that such biases predict patient functioning. The forth study examined the degree to which a successful cognitive-behavioural program was able to modify the observed attentional bias towards sensory pain words. Forty-two patients with chronic pain conditions for more than three months were recruited prior to commencing a cognitive-behavioural pain management program. Participants were assessed before the program, after the program and at one-month follow-up. Results confirmed that chronic pain patients exhibited biased attention towards sensory pain-related words at pre-treatment. These biases were still evident at post-treatment, but were no longer statistically significant at follow up. Multiple regression analyses indicated that the changes in attentional bias towards sensory words between post-treatment and follow-up were predicted by pre- to post- treatment changes in fear of movement (Tampa Scale for Kinesiophobia) but not other relevant variables, such as fear of pain or anxiety sensitivity. These results demonstrate that successful cognitive-behavioural treatments can reduce selective attention, thought to be indicative of hypervigilance towards pain. Moreover, these biases appear to be changed by reducing the fear associated with movement. Theoretically, these results provide support for the fear of (re)injury model of pain. Clinically, this study supports the contention that fear of (re)injury and movement is an appropriate target of pain management and that reducing these fears causes patients to attend less to pain-related stimuli.

Systemic lupus erythematosus (SLE) is a relatively rare autoimmune disease with no known aetiology or cure. In addition to numerous physical symptoms, those living with SLE have also been shown to experience significant emotional and psychosocial difficulties. There has been little psychological research into SLE despite the rapidly increasing interest in health psychology and quality of life issues over the last two decades. One such issue that has commanded particular attention is that of cognitive bias in individuals with chronic pain and/or chronic illness. Cognitive bias toward illness-related information is theorised to indicate the presence of an illness self-schema, and is a valuable tool of investigation as it permits access to a level of cognitive structure that is inaccessible via self-report instruments. The primary focus of the present study is to investigate recall bias for pain- and illness-related words in SLE patients. This bias is explored relative to the recall of neutral words and depression-related words, and also relative to the responses of rheumatoid arthritis (RA) patients and healthy controls. Two hypotheses are proposed: firstly, that bias is related to disease activity; and secondly, that bias is related to the combination of illness and depression. The findings provide support for the second hypothesis, with the additional caveat that the nature of the pain/illness stimuli used is important in determining the presence of cognitive bias. No recall bias for illness-related words as a whole was found in any of the groups, nor was there evidence of a recall bias in the SLE and RA patients when they were divided according to depression status. However, when the illness words were examined separately according to �sensory pain� and �disability-related� words, a clear bias for disability words was found in the depressed patient group. It is concluded that there is a relationship between depression in chronically ill individuals, and the way in which such individuals process disability-related words. In accordance with the schema-enmeshment model (Pincus & Morley, 2001), it is suggested that both a pain-schema and an illness-schema exist, and it is when these two schemas become enmeshed with the self-schema that depression occurs in chronic pain/chronically ill patients. The cognitive bias assessment paradigm adopted in this study-one that is typically used in similar investigations-is lengthy, requires sophisticated equipment and can be difficult to interpret on an individual level. The present study investigates the relationship between cognitive biases in SLE patients and a recently-developed task, PRISM, which appears to symbolise the enmeshment of illness-, pain- and self-schemas. Analyses confirmed that recall of negative illness words was the only independent predictor of PRISM scores. This suggests that PRISM, a quick and easy task to administer, may have considerable usefulness as a clinical tool to assess information relevant to the enmeshment of illness- and self-schema. A greater understanding of schema and the processing styles of chronically ill patients will allow for more effective psychological treatment such that quality of life can be improved.

Chronic Fatigue Syndrome (CFS) is a contested condition that generates scepticism and occupies a marginalised position within medical and social contexts. The thesis examines the illness experiences, and specifically the experiences of self, for people affected with CFS. Using qualitative inquiry, a substantive theory related to the process of self-renewal and adaptation associated with CFS is explicated. The theory encompasses the trajectory of CFS from onset to chronicity, and in exceptional instances, recovery. Illness narratives were derived from in-depth, semi-structured interviews of 19 adults, including 16 people affected with, and 3 people recovered from, CFS. Data was coded and analysed using a grounded theory approach. Analysis generated two parallel narratives that defined the illness experience of CFS: the narrative of the illness biographies and the narrative of self, specifically the struggling and diminished self seeking renewal. The illness biographies encompassed the stories of symptoms and their explanations, the encounters that ensued and their contentious milieu. The narrative of self was the primary narrative. It articulated the negative consequences to self and personhood associated with CFS, named the Violation of Self, and the consequent efforts of participants to decrease the struggle and violation by use of the Guardian Response and the Reconstructing Response. The Guardian Response provided protection and self-reclamation. The Reconstructing Response fostered self-renewal and meaning. The two narratives were bridged by the threats of CFS. That is, the illness biographies were accompanied by threats of disruption related to chronic illness, and by threats of invalidation that arose from CFS as a contested condition. In turn, these threats provided the catalyst to the violation and responses as described in the narrative of self. Under different conditions the relative strengths of violation, guardianship or reconstruction fluctuated, and it was these fluctuations that presented the participants with the ongoing struggle of CFS.

No description available.

Thesis (Ph. D.)--University of Washington, 1989. / Vita. Includes bibliographical references.