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dc.contributor.advisorVickers, James
dc.contributor.authorWatkins, Jennifer
dc.date.accessioned2010-05-11T15:52:13Z
dc.date.available2010-05-11T15:52:13Z
dc.date.issued2010
dc.identifier.urihttp://hdl.handle.net/2436/98533
dc.descriptionA thesis submitted in partial fulfilment of the requirements of the University of Wolverhampton for the degree of Master of Philosophy
dc.description.abstractPlatelets are known to play a key role in acute coronary events, such as myocardial infarction, associated with advanced atherosclerosis, but a number of papers have recently been published suggesting that platelet adhesion may initiate atherosclerotic lesion formation. The proposed research aimed to investigate this by seeing whether platelet adhesion occurred, directly or via leukocytes, to the endothelium in diabetic conditions. Diabetic-like conditions were chosen because an accelerated rate of lesion formation occurs. This was achieved by incubating endothelial cells with high concentrations of glucose and various types of AGEs. Bovine serum albumin of different purity, a peptide of albumin, and haemoglobin were glycated with D-glucose. Samples were taken at 2 weeks intervals to allow for determining the extent of glycation and allowing for investigation into whether the extent of glycation affected platelet adhesion. It also made possible analysis of extent of glycation, to see whether these have a relation to endothelial dysfunction (including cell proliferation, cell adhesion molecule expression, and ROS and cytokine production). There are discrepancies in the finding of studies looking into the effect of AGEs on the endothelium and there are no reported studies looking at cytokine production. As such, it was hoped that this research would allow for a greater understanding of the processes involved and whether endothelial dysfunction could account for accelerated lesion formation associated with diabetes. As a whole, the research intended to explore the hypothesis that platelet adhesion to the endothelium is required for foam cell formation and their development into atherosclerotic lesions. It aimed to see whether hyperglycaemia and the presence of high levels of AGEs induces endothelial dysfunction and therefore increases monocyte adhesion by the presence of activated platelets. In doing so, a greater understanding of the processes involved in accelerated lesion formation would allow for targeted research to allow for treatments to reduce foam cell deposition. This could be the use of a cocktail of anti-platelet drugs or ones that reduce endothelial dysfunction. This would reduce the manifestation of cardiovascular disease and therefore improve diabetic patient life as well as reduce the cost of treatment for the NHS, and therefore for the tax payer.
dc.language.isoen
dc.publisherUniversity of Wolverhampton
dc.subjectPlatelet
dc.subjectAdhesion
dc.subjectEndothelial dysfunction
dc.subjectAtherogenesis
dc.subjectDiabetes
dc.subjectAtherosclerosis
dc.titlePlatelet adhesion in atherogenesis
dc.typeThesis or dissertation
dc.type.qualificationnameMPhil
dc.type.qualificationlevelMasters Degree
refterms.dateFOA2018-08-22T07:15:50Z
html.description.abstractPlatelets are known to play a key role in acute coronary events, such as myocardial infarction, associated with advanced atherosclerosis, but a number of papers have recently been published suggesting that platelet adhesion may initiate atherosclerotic lesion formation. The proposed research aimed to investigate this by seeing whether platelet adhesion occurred, directly or via leukocytes, to the endothelium in diabetic conditions. Diabetic-like conditions were chosen because an accelerated rate of lesion formation occurs. This was achieved by incubating endothelial cells with high concentrations of glucose and various types of AGEs. Bovine serum albumin of different purity, a peptide of albumin, and haemoglobin were glycated with D-glucose. Samples were taken at 2 weeks intervals to allow for determining the extent of glycation and allowing for investigation into whether the extent of glycation affected platelet adhesion. It also made possible analysis of extent of glycation, to see whether these have a relation to endothelial dysfunction (including cell proliferation, cell adhesion molecule expression, and ROS and cytokine production). There are discrepancies in the finding of studies looking into the effect of AGEs on the endothelium and there are no reported studies looking at cytokine production. As such, it was hoped that this research would allow for a greater understanding of the processes involved and whether endothelial dysfunction could account for accelerated lesion formation associated with diabetes. As a whole, the research intended to explore the hypothesis that platelet adhesion to the endothelium is required for foam cell formation and their development into atherosclerotic lesions. It aimed to see whether hyperglycaemia and the presence of high levels of AGEs induces endothelial dysfunction and therefore increases monocyte adhesion by the presence of activated platelets. In doing so, a greater understanding of the processes involved in accelerated lesion formation would allow for targeted research to allow for treatments to reduce foam cell deposition. This could be the use of a cocktail of anti-platelet drugs or ones that reduce endothelial dysfunction. This would reduce the manifestation of cardiovascular disease and therefore improve diabetic patient life as well as reduce the cost of treatment for the NHS, and therefore for the tax payer.


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