Thesis (Ph. D.)--University of Rhode Island, 2003. / Typescript. Includes bibliographical references (leaves 69-77).

Thesis (Ph. D.)--Rutgers University, 2008. / "Graduate Program in Psychology." Includes bibliographical references (p. 58-62).

Thesis (M.A.)--Marquette University, 2010. / Available for download on Dec. 7, 2010. John F. LaDisa, Lars Olson, Joseph Cava, Margaret Samyn, Kimberly Gandy, Laura Ellwein, Advisors.

Thesis (M.S.)--University of Wisconsin--Madison, 1984. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 41-43).

Thesis (M.S.)--University of Wisconsin--Madison, 1982. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 68-71).

M.Cur. (Intensive General Nursing) / The rehabilitation of the coronary artery bypass patient should be a continuation of the contact which exists during the hospitalisation phase, with specific reference to the pre-dismissal phase. As a member of the health team, the nurse makes the most important inputs during this phase because she is the one who is in constant contact with the patient and his family. The purpose of this study is to determine, by means of set criteria and within a nursing perspective, the contributions that are made by various support groups to the rehabilitation of persons who have undergone coronary artery bypass surgery.

M.A. (Clinical Psychology) / This research was undertaken in an attempt to validate the hypotheses that depression reported after coronary artery bypass grafting could be attributed to cognitive distortion, learned helplessness and loss of appropriate social reinforcement. Thirty subjects from the J.G. Strijdom Hospital in Johannesburg were randomly selected from a population of 80 patients who had undergone their first coronary artery bypass graft and assessed for depression and the related dimensions of the hypotheses. Mood was also assessed. On the basis of Beck Depression Inventory scores, 17 subjects were divided into experimental and control groups of depressed and non- depressed patients. The differences between the two groups were then compared. Overall, no support was found for the learned helplessness, cognitive distortion or loss of social reinforcement hypotheses, although fatigue, sadness and egotism were found to be the most significant differences between depressed and non-depressed post-operative patients. Contrary to indications in the literature, only 40 percent of patients in this study were found to be clinically depressed. The findings of this research may be seen to offer support for the "coronary-prone Behaviour" hypothesis, suggesting post-operative psychotherapeutic programmes for coronary artery bypass graft patients should address themselves to changing the behavioural styles of these patients both pre- and post-operatively.

Percutaneous coronary intervention with stent deployment is the dominant form of revascularisation for patients with coronary artery disease. Although drug-eluting stents have reduced the incidence of instent restenosis, they are associated with late problems related to delayed vascular healing including late stent thrombosis. The use of gene-eluting stents offers the potential to deliver localised gene therapy to the vascular wall with the aim of both reducing restenosis and promoting endothelialisation. Two candidate genes were investigated. Connective tissue growth factor (CTGF) promotes smooth muscle cell apoptosis and stimulates endothelial growth in vitro, and has an integral role in wound healing. Fibromodulin (FMOD) is involved in collagen metabolism and is a key mediator of scarless wound healing. Both genes have previously been shown to suppress restenosis in an ex vivo vein graft model. Plasmids containing these two genes were constructed with an expression cassette specially designed to maximise transgene expression in vascular smooth muscle cells. These plasmids were coated onto coronary stents with a polymer and the effects of these gene-eluting stents were investigated in an in vivo pig coronary artery model. Previous work by our group has suggested that systemic -blockade can affect the degree of transgene expression from viral vectors, and experiments were also performed to investigate the effect of β-blockers on plasmid-mediated gene expression. At 28 days there was no significant difference in angiographic late loss or neointimal hyperplasia between the groups treated with stents coated with FMOD or CTGF and the group treated with stents coated with the marker gene lacZ. This lack of efficacy appeared to be as a result of extremely poor transgene expression rather than due to a genuine failure of the transgenes to elicit a relevant biological effect. There was no difference in in vivo gene expression demonstrated as a result of β-blockade, but again this result was probably due to limited transgene expression. The potential causes of poor transgene expression in this study are reviewed and future directions for research on plasmid-mediated gene therapy are considered.

The first genetic CAD risk locus to be identified by genome-wide association studies, single nucleotide polymorphisms (SNPs) at 9p21.3 predispose to increased risk of CAD. By bioinformatics scan analysis of the 9p21.3 locus; we interrogated the 59 linked SNPs over the 53,202bp to identify putative transcription factor-binding consensus sequences. We hypothesize that some genetic polymorphisms at the 9p21.3 locus are functional and will disrupt specific regulatory sequences within enhancers. Here, I investigated how polymorphisms affect TEAD-dependent regulation at the 9p21.3 locus, and also how polymorphisms affect GATA factor-dependent regulation at the 9p21.3 locus, using cultured HEK293 and primary human aortic smooth muscle cells (HAoSMCs) to transfect the pGL3-promoter plasmid constructs containing the reference or risk variant sequences (rs10611656, rs4977757, rs10757269, rs9632885). We showed by luciferase reporter assay that the risk allele of the SNPs disrupt activation by various TEAD transcription factors. We also performed electrophoretic mobility shift assay (EMSA) to test for allele-specific transcription factor binding that affect the family of TEAD transcription factors and the GATA factors. EMSA showed binding of TEAD3 and TEAD4, and differential binding for both GATA genotypes, and luciferase reporter assay confirmed that TEAD3 and TEAD4 activate the non-risk but not the risk allele, and for GATA factors no significant activation was shown. Our investigations lead us to conclude that rs10811656 and rs4977757 are functional and disrupt specific TEAD regulatory sequences within enhancers

Toxicity preventing activity (TxPA) is a recently identified substance in serum which counteracts the toxic effect of very low density lipoproteins upon endothelial cells in vitro. In two clinical studies, TxPA was low in individuals with angiographically demonstrable coronary artery disease. An atherogenic index which combines TxPA with lipoprotein cholesterol values classifies individuals with coronary artery disease with an accuracy of greater than 93%. TxPA precipitates with 0.15 M trichloroacetic acid and above 3 M (NH4)2SO4. Activity is present in Cohn fractions IV4 and V and is stabilized by antioxidants. TxPA co-lutes with the albumin peak on gel filtration chromatography and as a subcomponent of albumin on ion-exchange chromatography. Isoelectric focusing resolves albumin into two major peaks with pI values of 4.8 and 5.6. The TxPA is identified as the pI 5.6 albumin peak.