Thesis (M.Med.(Diagnostic Radiology))--University of the Witwatersrand, Faculty of Health Sciences, 2000.

Graduation date: 2006

No description available.

Thesis (doctoral)--Lund University, 1998. / Added t.p. with thesis statement inserted.

Thesis (doctoral)--Lund University, 1998. / Added t.p. with thesis statement inserted.

AAA disease remains a common and life threatening condition, predominantly affecting men of retirement age. Whilst clinical studies have done much to predict the course of this disease, understanding the pathogenesis has been complicated by both a multi-factorial aetiology as well as several poorly defined stages to the disease (formation, growth and rupture). Evidence points to a considerable inheritable component to this condition, but as yet, associations with identified genetic variants are few and weak. This thesis describes the current understanding of the molecular mechanisms behind AAA pathogenesis, concentrating on aneurysm formation and growth. A meta-analysis of published candidate gene studies identified three genes with small but significant effects on risk of developing AAA (ACE, MTHFR and MMP9) and none with a significant effect on AAA growth. Further examination of five genes connected the Renin-Angiotensin System, using three distinct case control series, demonstrated the strongest reported association to date with AAA disease risk, with AGTR1+1166A>C. (OR 1.55 [1.30-1.83, p=5x10-7]). An interest in the role of the TGF-β pathway in AAA formation and growth has developed from the recent illumination of the mechanism behind aneurysm aetiology in Marfan syndrome. Haplotype analysis was used to investigate five genes coding for TGF-β and its binding protein (LTBP). Variants in TGFB3 and LTBP4 were significantly associated with altered AAA growth. The importance of inflammatory process was also supported by observations made in a very large longitudinal data set of AAA growth. Anti-inflammatory drugs, together with anti-platelet drugs and drugs used in diabetes, were significantly associated with decreased AAA growth independent of confounding factors. In conclusion, this thesis demonstrates; a role for the RAS in AAA formation; TGF-β in AAA growth; and anti-inflammatory drugs as potentially disease modifying. In addition, observations have also been made concerning a two tier effect illuding to the nature AAA progression.

No description available.

Zhu Xian Lun. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1991. / Includes bibliographical references (leaves 83-103). / ACKNOWLEDGEMENT --- p.1 / ABSTRACT --- p.2 / Chapter CHAPTER 1 --- INTRODUCTION --- p.4 / Chapter CHAPTER 2 --- TREATMENT METHODS OF INTRACRANIAL ANEURYSMS OTHER THAN CLIPPING --- p.6 / Chapter CHAPTER 3 --- EXPERIMENTAL ANEURYSM MODELS --- p.24 / Chapter CHAPTER 4 --- A SUITABLE ANEURYSM MODEL FOR THE STUDY --- p.30 / Introduction / Materials and methods --- p.31 / Results --- p.37 / Discussion --- p.46 / Conclusion --- p.56 / Chapter CHAPTER 5 --- REINFORCEMENT AND FILLING TREATMENT IN EXPERIMENTAL ANEURYSMS --- p.57 / Introduction / Materials and methods --- p.58 / Results --- p.63 / Discussion --- p.71 / Conclusion --- p.77 / Chapter CHARTER 6 --- SUMMARY --- p.79 / Chapter APPENDIX I --- REFERENCES --- p.83 / Chapter APPENDIX II --- TABLES --- p.104 / Chapter APPENDX III --- FIGURES --- p.115

Currently, size is used as the predetermining factor to judge whether a saccular aneurysm is likely to rupture. Recent studies of the nonlinear mechanics of saccular aneurysms suggest that it is unlikely that they enlarge or rupture via material (limit point) or dynamic (resonance) instabilities. Rather, there is a growing body of evidence from both vascular biology and finite element analyses that implicate mechanosensitive growth and remodeling processes. There is, therefore, an even greater need to quantify regional multiaxial wall stresses, which because of the membrane-like behavior of aneurysms implicates the need for better data on regional surface curvatures. By using a convenient function, such as a Legendre polynomial, a quick, accurate approximation can be made for the size and shape of a saccular aneurysm that allows for stress analysis that surgeons can use to determine if the risk of rupture warrants the risk of treatment.

Currently, size is used as the predetermining factor to judge whether a saccular aneurysm is likely to rupture. Recent studies of the nonlinear mechanics of saccular aneurysms suggest that it is unlikely that they enlarge or rupture via material (limit point) or dynamic (resonance) instabilities. Rather, there is a growing body of evidence from both vascular biology and finite element analyses that implicate mechanosensitive growth and remodeling processes. There is, therefore, an even greater need to quantify regional multiaxial wall stresses, which because of the membrane-like behavior of aneurysms implicates the need for better data on regional surface curvatures. By using a convenient function, such as a Legendre polynomial, a quick, accurate approximation can be made for the size and shape of a saccular aneurysm that allows for stress analysis that surgeons can use to determine if the risk of rupture warrants the risk of treatment.