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dc.contributor.authorSvedlund, Elin
dc.date.accessioned2016-02-10T13:03:30Z
dc.date.available2016-02-10T13:03:30Z
dc.date.issued2016-02-10
dc.identifier.urihttp://hdl.handle.net/2077/41828
dc.description.abstractDegree Project Thesis, Programme in Medicine. TITLE: A mouse model of myocardial infarction in Filamin B deficient mice. Abstract Background Myocardial infarction (MI) is the most common endemic disease and the condition is the leading cause of death in all industrialized countries. Animal models of MI plays a significant role in the development of diagnosis and therapeutic strategies in human MI, as it enables studies of pathobiological and pathophysiological mechanisms. A mechanism that could be interesting as a therapeutic strategy to treat cardiovascular diseases is the induction of angiogenesis. The protein FLNB has been shown to stimulate angiogenesis and it is therefore interesting to investigate its effects on the myocardium post MI since neovascularization is crucial for the healing process. Objectives My first aim was to develop a method of inducing MI in mice. My second aim was to use the method to induce MI in FLNB deficient mice and in wild types in order to examine differences between the groups regarding the ischemic injury. Methods When the method was established a baseline echocardiography was performed one day prior to surgery. The echocardiography procedure was repeated at three time points in order to quantify the area of infarction. Ten weeks post-surgery the hearts were fixed for histological sections and staining. Survival, cardiac function and healing process were analyzed. Results and discussion The protocol of permanent ligation of LAD at the atrioventricular junction ensured a statistically significant and reproducible MI. No difference in size of the infarct area between the groups was indicated by the analysis but the experiment needs to be repeated with a larger number of animals in order to obtain significant statistical basis. A Fisher Exact test suggested that wild-type mice survive myocardial injury to a greater extent than the mice that are partly deficient of FLNB. Although, death occurred during the critical days post-surgery and no conclusion about survival can therefore be drawn.sv
dc.language.isoengsv
dc.subjectmyocardial infarctionsv
dc.subjectFilamin Bsv
dc.titleA mouse model of myocardial infarction in Filamin B deficient micesv
dc.title.alternativeA mouse model of myocardial infarction in Filamin B deficient micesv
dc.typeText
dc.setspec.uppsokMedicine
dc.contributor.departmentUniversity of Gothenburg / Institute of Medicineeng
dc.contributor.departmentGöteborgs universitet / Institutionen för medicinswe
dc.type.degreeStudent essay


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