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This thesis explores the relationship between memory self-report, depression and neuropsychological performance at both baseline and six months following coronary artery bypass graft surgery (CABG). An additional important refinement on previous work included the adoption of a theoretically driven approach to calculate post-test change scores (Standardized Based Regression) in order to control measurement error, practice effects and regression-to-the-mean. A further important refinement included the analysis of different subtypes of depression and how they affect patient perceptions of memory over time. A prospective study of 64 elective CABG surgery patients (mean age 65.4 years) was undertaken pre-operatively and six months post-operatively, along with the assessment of 50 normal control participants (mean age 68.6 years). The neuropsychological test battery was selected in accordance with the Statement of Consensus on the Assessment of Neurobehavioural Outcomes after Cardiac Surgery (Murkin et al., 1995). Standardized self-report measures of depression and memory self-report were also included, namely the DASS and MAC-S. Unexpectedly, results showed that both CABG patients and controls scored in the 'normal' range for depression at both testing intervals. However, at baseline assessment, analyses showed small, significant correlations between memory self report and depression as well as between memory self-report and the CVLT variable Short Delay Free Recall. The depressive subscales of Inertia and Self-deprecation also emerged as significant predictors of memory self-report using hierarchical regression analysis. At follow-up assessment, no significant correlations were found between memory self report, depression or any neuropsychological variable. However, the DASS depression subscale of Devaluation of Life entered as a significant predictor of memory self-report. Collectively, these results provide little evidence of a relationship between subjective and objective measures of memory. However, they indicate that relatively non-depressed patients can show mild variants of the cognitive biases and symptoms classically related to clinical depression and that these symptoms correlate significantly with perceptions of memory. Although no consistent trends were found over time, excluding any inferences of causality, this study was the first to systematically examine the relationship between depressive symptoms and memory self-report, with a view to assisting clinicians to identify patients more inclined to over-report memory failure. / Thesis (PhD)--University of South Australia, 2006.

Thesis (MClinPharm)--University of South Australia, 1997

Angina pectoris (AP) is an important manifestation of chronic coronary heart disease, estimated to affect more than 10% of people aged over 60 years. Typically, AP is experienced as chest pain, induced by exertion and relieved by rest or medication. Despite contemporary medical management, people with chronic AP may experience symptoms during everyday activities. Accordingly, AP has significant potential to limit people's daily activities and participation in life roles. Yet there is a limited literature reporting the impact of AP on activities. The aim of this program of research was to describe the relationship between AP and limitation in people's activities and participation in life roles. The research comprised three studies. The first two studies were undertaken by secondary analysis of data from a large population study, the Australian Longitudinal Study of Ageing (ALSA). These studies answered research questions about the relationship between AP and activity limitation in a large sample of older Australians. The third study involved the collection of new data to explore how people of various ages perceive and manage the impact of AP on their activities and life roles. / PhD Doctorate

Heart failure has a significant impact on mortality and morbidity. Dilated cardiomyopathy (DCM) is the third most common cause of heart failure and the most common reason for heart transplantation. Familial DCM is known to be caused by mutations in the LMNA gene encoding lamins A and C. New methods to enhance cardiac contractility would be beneficial in the treatment or prevention of heart failure. The focus of this thesis was to evaluate the mechanisms of altered contractility in two mouse models: the LMNA knockout model (homozygous, Lmna-/-; heterozygous, Lmna+/-) generated by targeted deletion of the lmna gene, and the model of enhanced contractility due to cardiac alpha1A-adrenergic receptor (???1A-AR) overexpression (A1A1). Previous studies have found altered nuclear-desmin connections in lamin A/C deficient mice. It was proposed that these alterations result in ???defective force transmission???, which leads to DCM. Studies in this thesis have supported this hypothesis. Studies of isolated single cardiomyocytes from mice aged 4-6 weeks demonstrated abnormal cell morphology and contractile dysfunction in Lmna-/- cardiomyocytes, while Lmna+/- cells showed no overt phenotype. Excitation-contraction coupling experiments and forcecalcium studies in skinned fibers excluded altered calcium kinetics as a primary cause of DCM in this model, but there was evidence of reduced sarcomere numbers and reduced sarcomere lengths as a contributor to reduce force generation in Lmna-/- and Lmna+/- mice. Previous in vivo studies showed that A1A1 mice had enhanced contractility with the absence of hypertrophy. Studies on isolated single cardiomyocytes from A1A1 mice aged 8-12 weeks showed reduced contractility in the absence of ???1A-AR stimulation, but an exaggerated response to ???1A-AR stimulation. In contrast isolated isovolumic Langendorff perfused A1A1 hearts without ???1A-AR stimulation replicated the enhanced contractility observed in vivo. These studies are consistent with down-regulation of contractility due to the hyperactivity of the overexpressed ???1A-AR in vivo, which only becomes evident in isolated cells without ???1A-AR stimulation due to the loss of functional receptor numbers during isolation. Sufficient spontaneously active ???1A-ARs are preserved in the isolated Langendorff heart preparation to ensure maximum contractility driven by increase calcium release.

Antenatal fetal surveillance is a field of increasing importance in modern obstetrics. Measurements extracted (such as fetal heart rate) from antenatal fetal monitoring techniques have the potential to reduce the social, personal and financial burdens of fetal death on families, health care systems and the community. Techniques to monitor the fetus through pregnancy have been developed with the aim of providing information to enable the clinician to diagnose fetal wellbeing, characterise development and detect abnormality. An early diagnosis before delivery may increase the effectiveness of the appropriate treatment. Over the years, various research efforts have been carried out in the field of fetal electrocardiography by attaching surface electrodes to the maternal body. Unfortunately the desired fetal heartbeat signals at the electrode output are buried in an additive mixture of undesired interference disturbances. In this thesis, a non-invasive fetal electrocardiogram machine has been designed, constructed and implemented. This machine is composed of three modified electrocardiogram circuits and an external soundcard. Data was acquired from four surface electrodes placed on the maternal body. Eleven pregnant subjects, with a gestation age between the 30th and 40th weeks of pregnancy, were used to investigate the validity of this machine. Fetal R-waves were detected in 72.7 percent of subjects. The development of a non-invasive machine, capable of detecting and recording valuable anatomic and electrophysiological information of a fetus, represents an important tool in clinical and investigative obstetrics.

Title page, table of contents and abstract only. The complete thesis in print form is available from the University of Adelaide Library. / Nitric oxide (NO) plays a fundamental role in vascular homeostasis including vasomotor tone, platelet adhesion and aggregation. The current studies examine various aspects of NO responses, including: the methodology for assessment of vascular NO responses, and identification of factors reponsible for poor responsiveness and pharmacological modulation of these responses. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1277081 / Thesis (Ph.D.) -- University of Adelaide, School of Medicine, 2007

[Truncated abstract] Cells need to be able to detect changes in their surrounding environment and transduce these signals into the appropriate cellular compartments. One of the major ways that the cell achieves this signal transduction is through the process of phosphorylation. Protein kinases are the enzymes responsible for catalysing this transfer of phosphate groups from ATP to amino acid residues of their specific substrates. A subfamily of serine/threonine kinases known as the Mitogen-Activated Protein Kinases (MAPKs) is essential in a diverse range of cell processes including growth, metabolism, differentiation and death. The first identified MAPKs, the Extracellular Signal-Regulated Kinases (ERKs), were found to be activated in response to mitogenic stimuli such as growth factors. However, since the discovery of the ERKs, other pathways leading to the activation of related kinases have been recognised. These kinases are preferentially activated in response to stress, and are thus termed “Stress-Activated Protein Kinases” or SAPKs. They consist of the c-Jun N-terminal kinase isoforms 1, 2 and 3 (also called SAPK1γ, SAPK1α and SAPKβ respectively) and the p38 MAPKs, p38α, p38β, p38γ and p38δ (also called SAPK2a, SAPK2b, SAPK3 and SAPK4 respectively). A major challenge in this field has been to identify the substrates and functions of the SAPKs. This has been partly achieved by the development of inhibitors for the JNK MAPKs and SAPK2a/b. However, no inhibitors currently exist that specifically inhibit SAPK3 and SAPK4. Therefore, elucidating the function of these SAPKs has proved more difficult. Recent studies suggest that SAPK3 may play a unique role in the cell compared to other members of the p38 MAPK family. For example, several signalling proteins appear to specifically activate SAPK3 in certain circumstances while not activating other members of the p38 MAPK family. In addition, SAPK3 contains a unique sequence motif that allows it to bind to specialised domains known as PDZ domains. The interaction of SAPK3 with proteins containing these domains may regulate its subcellular localisation and interactions with other proteins in the cell. This project was undertaken to expand the knowledge on the expression, localisation, substrate specificity and binding partners of SAPK3. In Chapter 3 of this thesis, a SAPK3 monoclonal antibody was evaluated for its ability to specifically recognise endogenous SAPK3 protein. SAPK3 was found to be expressed in immortalised cell lines and primary cultures of neonatal rat myocytes, and to be colocalised with the mitochondria of these cells. This co-localisation remained unaltered in response to treatment with the nuclear export inhibitor Leptomycin B, and with exposure to osmotic shock, suggesting that SAPK3 substrates may be localised at the mitochondria

Thesis (Ph. D.)--Virginia Commonwealth University, 2007. / Prepared for: School of Nursing. Bibliography: leaves 120-145. Also available online.

Thesis (Ph. D.)--University of Adelaide, Dept. of Applied Mathematics, 1987. / Includes bibliographical references (leaves 184-190).