230 leaves : / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (M.D.)--University of Adelaide, Dept. of Psychiatry, 1976

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<p>Increasing diabetes prevalence rates, poor involvement of and limited knowledge among health care professionals in disease management, and poor implementation of guidelines are barriers to quality diabetes care. This thesis aimed to develop, implement and evaluate an on-site diabetes pharmacotherapy program for public sector pharmacists. Qualitative and quantitative research methods were used inthe pre- and post-intervention study.</p>

The prevalence of Type 2 diabetes mellitus is increasing worldwide and with it, the demands on heath service resources. As the long-term outcomes of this disease are dependent upon reducing lifestyle risk factors, together with effective treatment and screening strategies, much of the responsibility for diabetes management ultimately resides with the patient. Therefore patient education is a key part of the care of this population. A trial of an empowerment based health education programme was underpinned by the theories associated with health protective behaviour and those associated with adult learning. These align patient education to an experiential learning process within which beliefs about self-efficacy and the effects of social-environmental influences are central to outcomes. This view was compatible with current health care policies which see patients taking a more active and informed role in their disease management. The trial utilised a randomised controlled wait-list design to allow for the ethical limitations of excluding patients from educational treatment, and permitted collection of data over a short- and long-term period. A qualitative approach to data collection, using symbolic interactionism, was also integrated into the clinical trial. The two types of data were treated as complementary so that the outcomes of the trial relied upon detailed exploration of how they complemented each other. Eighty-nine patients were recruited from three diabetes centres. All patients recruited were blindly randomised to a 'Look After Yourself education programme. Clinical, behavioural and psychological outcomes were measured at six and twelve months. The relationship between these, the content of the intervention and participants' perspectives was assessed through ten focus group interviews. The combined results showed that the educational intervention had modified participants' personal models of diabetes by increasing their knowledge and understanding, by clarifying their beliefs and by changing their attitudes toward the disease and its management. It facilitated the acquisition of skills and prompted movement into the behaviour change cycle for the majority of those taking part, regardless of socio-economic status. The impact of these changes upon clinical outcomes was most effective where participants perceived their risk factors to be greatest. These findings supported the production of a framework for guiding nursing intervention to enhance patient self-management of diabetes. To adhere to such a model of care, however, the trial highlighted the need to expand the biomedical orientation to patient education so that it allows for patients' self-perceived needs. This demands integration of the medical and behavioural sciences into the practice of diabetes care and recognition of the need to support patients in their lifelong task of maintaining their own health. It recognises that care for chronic illness is an inherently different social enterprise than is care for acute illness. The findings have therefore highlighted the training needs for health professionals so that they can develop the skills that can enhance this process. Whilst these conclusions acknowledge the importance of continuing education and support for patients, such clinical practice will rely upon tailoring nursing intervention to the outcomes of a diabetes-specific assessment instrument. In this way, educational referral can become an integral part of a patient's treatment profile. Only then might health professionals authenticate a culture that supports patient choice so that they can take greater control over their health.

<p>Increasing diabetes prevalence rates, poor involvement of and limited knowledge among health care professionals in disease management, and poor implementation of guidelines are barriers to quality diabetes care. This thesis aimed to develop, implement and evaluate an on-site diabetes pharmacotherapy program for public sector pharmacists. Qualitative and quantitative research methods were used inthe pre- and post-intervention study.</p>

Rosuvastatin treatment prevented diabetic deficits in endothelium-dependent relaxation to acetylcholine of mouse aorta and cavernosum, and prevented diabetic deficits in NANC-mediated relaxation, in the presence of atropine and guanethidine, of rat and mouse cavernosum precontracted with the adrenergic agonist phenylephrine. Similarly, rosuvastatin partially reversed established diabetic deficits of endothelium-dependent relaxation of mouse aorta and cavernosum, and NANC-relaxation of mouse cavernosum. However, plasma lipids were unaltered by either diabetes or rosuvastatin treatment in mice, indicating that the beneficial actions of the statin were not dependent on lipid-lowering. Co-treatment with mevalonate, the product of HMG-CoA redustase, ameliorated the beneficial actions of rosuvastatin confirming that the effects were dependent on cholesterol biosynthesis pathway inhibition. The endothelium and NANC-dependent responses of the isolated tissues were dependent on the production of nitric oxide (NO), as they were abolished following tissue incubation with the non-specific NO synthase (NOS) inhibitor <i>N</i>^G-nitro-L-arginine. As specific inhibitors for the endothelial, neuronal and inducible NOS isoforms are lacking, the secondary aim of this thesis was to investigate the specific roles of the NOS isoforms on aortic and cavernosal function of mice lacking the respective NOS genes (NOS KO's). The variations in response from NOS KO aorta and cavernosum were multiple, however, taken together suggest that mice lacking specific NOS isoforms develop compensatory mechanisms to retain NO-dependent functions. In summary, this thesis demonstrates that vascular and nervous NO-dependent functions can be improved by rosuvastatin therapy in diabetic rodents and that further investigation of the roles of the specific NOS isoforms may lead to therapeutic approaches for diabetes mellitus.

Single channel recordings from CRI-G1 insulin-secreting cells were used to characterize a novel ion channel. The presence of both Ca²⁺ and β-NAD⁺ at the cytoplasmic aspect of the membrane are required for channel activity. This is the first ion channel described which requires internal β-NAD⁺ for activity (thus termed NS_NAD). The channel was found to be permeable to all monovalent (Na⁺, K⁺and Cs⁺) and divalent cations tested (Ca²⁺, Mg²⁺, Ba²⁺, and Mn²⁺). The slope conductance is relatively large (70 - 90pS) compared to other non-selective cation channels and also has extremely slow kinetics (open and closed times in the range of seconds). Whole-cell voltage clamp experiments illustrate that internal β-NAD⁺ activates a cation current consistent with activation of the NS_NAD channel. Similar to the single NS_NAD channel, the β-NAD⁺-activated current was sensitive to the internal concentrations of both Ca²⁺ and β-NAD⁺. The non-selective nature of this cation current was confirmed by replacement of the internal K⁺ with Cs⁺ which did not diminish the β-NAD⁺-activated current. Additionally, replacement of external cations with the impermeant NMDG abolished the β-NAD⁺-activated current. The diabetogenic agent alloxan was found to irreversibly depolarize CRI-GI cells by opening a non-selective cation channel with characteristics similar to the NS_NAD channel. The channel activated by alloxan is characterized by a slope conductance of approximately 70 pS and very slow (seconds) kinetics. Channel activity is lost upon excision of the patch, but can be re-activated by the application of internal β-NAD⁺. The mechanism of alloxan-induced depolarization and channel activation appears to be through the production of reactive oxygen species (ROS). This data indicates that oxidative stress generated by both alloxan and H₂O₂ causes the activation of the NS_NAD channel which results in irreversible collapse of the membrane potential and massive Ca⁺ influx leading to eventual cell death. This may represent a component of the destruction of pancreatic β-cells during type I diabetes and possibly other pathologies in which oxidative stress is implicated.

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