Na reconstrução mamária com microcirurgia, a qualidade dos vasos, a proximidade com a região torácica e a anatomia constante são fatores relevantes na escolha do pedículo receptor. Apesar da grande aplicação clínica, os vasos toracodorsais e torácicos internos apresentam restrições como a imprevisibilidade da qualidade nas reconstruções tardias, as alterações do contorno do tórax e a inviabilidade de uma eventual revascularização futura do miocárdio. Com o desenvolvimento dos retalhos vascularizados por vasos perfurantes e o maior treinamento dos cirurgiões, novas alternativas de pedículos foram desenvolvidas. A preservação da cartilagem costal e dos vasos torácicos internos, bem como a maior exposição do campo operatório são mencionados como vantagens do emprego dos vasos perfurantes do músculo peitoral maior como receptor. Apesar da anatomia dos vasos perfurantes ter sido previamente estudada, são imprecisas as informações sobre sua origem e distribuição no tórax. Ademais, são escassos os dados relacionados à sua incidência e utilização nas reconstruções imediatas e tardias. Na presente investigação foram incluídos dois estudos: anatômico e clínico. No estudo anatômico avaliou-se a origem, distribuição e dimensões dos vasos perfurantes em 24 cadáveres frescos (48 regiões torácicas), por técnica de coloração e posterior dissecção. No estudo clínico analisou-se, 69 pacientes (77 reconstruções mamárias), sendo 46 imediatas e 31 tardias. Constatou-se no estudo anatômico 2,7 vasos perfurantes por região torácica, destes, 93% apresentaram pequeno e médio calibre e concentração preferencial no segundo espaço intercostal. Os vasos e o pedículo perfurante revelaram comprimento médio de 2,4 cm (1,0 a 3,2 cm) e 3,6 cm (2,1 a 4,5 cm), respectivamente. No estudo clínico, não foram observadas diferenças entre as pacientes submetidas à reconstrução imediata e tardia, quanto a idade (p=0,599), IMC (p=0,498), lateralidade da mama (p=0,671), hipertensão arterial sistêmica (p=0,732), diabetes (p>0,999) e tabagismo (0,828). Todavia, 61,3% das pacientes submetidas à reconstrução tardia relataram radioterapia previamente à cirurgia (p<0,001). Nas reconstruções imediatas, em 93,5% dos casos os vasos perfurantes estavam presentes e, em 37,2%, foi possível realizar as anastomoses. Entre as causas de insucesso das anastomoses destacaram-se a lesão vascular durante a mastectomia (48,8%) e a desproporção de calibre dos vasos (13,9%). Nas reconstruções tardias, em 12,9% dos casos, os vasos perfurantes estavam presentes e em nenhum caso foi possível realizar as anastomoses. A incompatibilidade de calibre dos vasos e a má qualidade da estrutura vascular foram as razões para não os empregar como pedículo receptor. Não foram observadas diferenças estatísticas quanto à incidência de complicações gerais (p=0,548), perda parcial do retalho (p=0,494), perda total do retalho (p=0,644) e necrose da pele remanescente da mastectomia (p=0,193) nas pacientes submetidas à reconstrução com pedículo receptor perfurante e com os demais pedículos receptores. Os resultados permitiram-nos concluir que a maior concentração de vasos perfurantes no segundo espaço intercostal e a distância entre 0,5 e 3 cm do esterno constituem parâmetros anatômicos importantes no planejamento da técnica. É recomendável que nas reconstruções imediatas se faça o planejamento prévio com o mastologista com intuito de preservar os vasos perfurantes, enquanto que nas reconstruções tardias, a presença de cirurgia prévia e da radioterapia podem se relacionar à menor reprodutibilidade da técnica / In breast reconstruction with microsurgery, the proper selection of the recipient pedicle is a significant factor for success. The compatibility of caliber and the uniform anatomy are the chief relevant factors in the choice of recipient vessels. Regardless of their broad clinical application, the thoracodorsal and internal thoracic vessels demonstrate limitations such as the unpredictable quality of late reconstructions, the changes in thoracic contour and the impairment for future coronary bypass. The progress of microsurgical technique and the development of perforator flaps has led to new recipient pedicle alternatives. Thus, sparing of the costal cartilages and the internal thoracic vessels as well as the wide surgical exposure are the main advantages of using the pectoralis major perforator vessels as recipient pedicles. Although the anatomy of the perforator vessels has been previously studied, the data about their origin and distribution is inexact. In addition, the data concerning their incidence and quality of immediate and late reconstructions are not available. In the present investigation, an anatomical and clinical study were performed. In the anatomical study, the origin, distribution and size of perforator vessels were evaluated in 24 fresh cadavers (48 thoracic regions) by staining technique and posterior dissection. The clinical study analyzed 69 patients (77 reconstructions), 46 immediate and 31 late reconstructions. The anatomic study observed 2.7 perforator vessels per thoracic region, with 93% presenting small and medium caliber and major concentration in the second intercostal space. The vessels and the perforator pedicles demonstrated an average length of 2.4 cm (1.0 to 3.2 cm) and 3.6 cm (2.1 to 4.5 cm) respectively. In the clinical study, no differences were observed between the immediate and late reconstructions regarding age (p=0.599), BMI (p=0.498), breast side (p=0.671), hypertension (p=0.732), diabetes (p>0.999) and smoking (0.828). Nevertheless, 61.3% of patients submitted to late reconstruction had radiotherapy prior to breast reconstruction (p<0.001). The perforator vessels were observed in 93.5% of the immediate reconstructions and vascular anastomosis was performed in 37.2%. Vascular injury during mastectomy (48.8%) and caliber compatibility (13.9%) were observed as the main causes of failure anastomosis. In late reconstructions, the perforator vessels were present in 12.9% and the anastomosis was impossible in all cases due to caliber differences and vascular quality. No statistical differences were observed regarding the incidence of general complications (p=0.548), partial loss (p=0.494), total loss (p=0.644) and mastectomy flap necrosis (p=0.193) in patients submitted to reconstruction with perforator vessels and the other recipient pedicles. The present study enabled us to conclude that the major concentration of perforator vessels in the second intercostal space and the distance between 0.5 and 3 cm from the sternal region represent an important anatomic parameter. In immediate reconstructions, a preoperative planning between the general and plastic surgeon is fundamental to preserve the main perforator vessels during the mastectomy. In late reconstructions the procedure was not demonstrable and some factors may be involved such as previous surgery and radiation therapy

"2+" in the title is superscript. / "December 2004." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2004. / Includes bibliographical references (p. 179-204) / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

Yang, Chao. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 137-146). / Abstracts in English and Chinese. / Thesis Committee --- p.i / Acknowledgements --- p.ii / Contents --- p.iii / Declaration --- p.vii / Abstract --- p.viii / 摘要 --- p.xi / Abbreviations --- p.xiii / Chapter CHAPTER ONE: --- INTRODUCTION / Chapter 1.1 --- Occurrence and Structure of Phytosterols in Plants --- p.P.1 / Chapter 1.2 --- Biological Effects of Phytosterols / Chapter 1.2.1 --- Cholesterol-lowering Effect of Phytosterols --- p.P.3 / Chapter 1.2.2 --- Anti-cancer Effect of Phytosterols --- p.P.5 / Chapter 1.2.3 --- Anti-proliferative Effect of Phytosterols --- p.P.5 / Chapter 1.3 --- Intake and Absorption of Phytosterols in Human Beings --- p.P.6 / Chapter 1.4 --- Occurrence and Physiological Levels of Phytosterol Oxidation Products (POPs) / Chapter 1.4.1 --- Occurrence of POPs --- p.P.8 / Chapter 1.4.2 --- Physiological Levels of POPs --- p.P.8 / Chapter 1.5 --- Endothelium and the Vascular Tone / Chapter 1.5.1 --- Role of Endothelium in the Control of Vascular Tone --- p.P.11 / Chapter 1.5.2 --- "Endothelial Dysfunction, Cholesterol Oxidation Products (COPs) and Phytosterol Oxidation Products (POPs)" --- p.P.12 / Chapter 1.6 --- Calcium Homeostasis in the Vascular Smooth Muscle Cells (VSMCs) / Chapter 1.6.1 --- Modes of Ca2+ Entry in VSMCs --- p.P.15 / Chapter 1.6.2 --- Modes of Ca2+ Efflux in VSMCs --- p.P.18 / Chapter 1.7 --- Objectives of the Study --- p.P.19 / Chapter CHAPTER TWO: --- β-SITOSTEROL OXIDATION PRODUCTS ATTENUATE VASORELAXATION BY INCREASING REACTIVE OXYGEN SPECIES AND CYCLOOXYGENASE-2 / Chapter 2.1 --- Introduction --- p.P.21 / Chapter 2.2 --- Materials and Methods / Chapter 2.2.1 --- Preparation of SOPs --- p.P.24 / Chapter 2.2.2 --- Gas Chromatography -mass Spectrometry (GC-MS) Identification of SOPs --- p.P.24 / Chapter 2.2.3 --- Analysis of SOPs --- p.P.25 / Chapter 2.2.4 --- Vessel Preparation --- p.P.25 / Chapter 2.2.5 --- Isometric Force Measurement --- p.P.26 / Chapter 2.2.6 --- Western Blotting --- p.P.27 / Chapter 2.2.7 --- Primary Culture of Rat Aortic Endothelial Cell --- p.P.28 / Chapter 2.2.8 --- Measurement of SOPs-induced Intracellular Oxidative Stress --- p.P.29 / Chapter 2.2.9 --- Drugs --- p.P.30 / Chapter 2.2.10 --- Data Analysis --- p.P.30 / Chapter 2.3 --- Results / Chapter 2.3.1 --- GC-MS Identification of SOPs --- p.P.32 / Chapter 2.3.2 --- Analysis of SOPs --- p.P.34 / Chapter 2.3.3 --- SOPs But Not β-Sitosterol Impaired ACh- and A23187-induced relaxations --- p.P.36 / Chapter 2.3.4 --- Inhibition of COX Pathway Reversed SOPs-induced Impairment in Relaxation --- p.P.39 / Chapter 2.3.5 --- SOPs Elevated Endothelial COX-2 Expression --- p.P.42 / Chapter 2.3.6 --- SOPs Increased COX-2 Expression via An Oxidative Stress-sensitive Pathway --- p.P.45 / Chapter 2.4 --- Discussion --- p.P.52 / Chapter 2.5 --- Conclusion --- p.P.56 / Chapter CHAPTER THREE: --- β-SITOSTEROL OXIDATION PRODUCTS POSSESS POTENTIAL VOCC BLOCKING EFFECT IN VSMCs / Chapter 3.1 --- Introduction / Chapter 3.1.1 --- 2+ Modes of Ca Entry and Efflux in Vascular Smooth Muscle Cells (VSMCs) --- p.P.57 / Chapter 3.1.2 --- Effect of Cholesterol and COPs on VSMCs --- p.P.57 / Chapter 3.2 --- Methodology and Materials / Chapter 3.2.1 --- Vessel Preparation --- p.P.59 / Chapter 3.2.2 --- Isometric Force Measurement iv --- p.P.59 / Chapter 3.2.3 --- Drugs --- p.P.60 / Chapter 3.2.4 --- Data Analysis --- p.P.61 / Chapter 3.3 --- Results / Chapter 3.3.1 --- SOPs but not β-Sitosterol Induced Relaxation in 60 mM K+ -preconstricted Endothelium-denuded Aorta --- p.P.62 / Chapter 3.3.2 --- Both SOPs and β-Sitosterol did not Relax U46619-preconstricted Endothelium-denuded Aorta --- p.P.64 / Chapter 3.3.3 --- Both SOPs and β-Sitosterol did not Relax PDA -preconstricted Endothelium-denuded Aorta --- p.P.66 / Chapter 3.3.4 --- SOPs Attenuated 60 mM K+-induced Contraction --- p.P.68 / Chapter 3.3.5 --- SOPs Attenuated Phenylephrine-induced Contraction --- p.P.70 / Chapter 3.3.6 --- Effect of SOPs on Concentration-dependent Responses to U46619 --- p.P.72 / Chapter 3.3.7 --- Preincubation with Bay K 8644 Abolished SOPs-induced Relaxation in 60 mM K+ -preconstricted Rings --- p.P.74 / Chapter 3.3.8 --- Preincubation with Thapsigargin did not Affect SOPs-induced Relaxation in 60 mM K+ -preconstricted Rings --- p.P.76 / Chapter 3.3.9 --- Preincubation with Ouabain did not Affect SOPs-induced Relaxation in 60 mM K+ -preconstricted Rings --- p.P.78 / Chapter 3.3.10 --- Preincubation with Nickel Potentiated SOPs-induced Relaxation in 60 mM K+ -preconstricted Rings --- p.P.80 / Chapter 3.4 --- Discussion --- p.P.84 / Chapter 3.5 --- Conclusion and Future Work --- p.P.88 / Chapter CHAPTER FOUR: --- INVOLEMENT OF NITRIC OXIDE IN THE PROTECTIVE EFFECTS OF PHYTOSTEROLS AGAINST HOMOCYSTEINE-INDUCED IMPAIRMENT OF ENDOTHELIUM-DEPENDENT RELAXATIONS OF RAT AORTA / Chapter 4.1 --- Introduction --- p.P.89 / Chapter 4.2 --- Materials and Method / Chapter 4.2.1 --- Vessel Preparation --- p.P.93 / Chapter 4.2.2 --- Isometric Force Measurement --- p.P.93 / Chapter 4.2.3 --- Western Blotting --- p.P.94 / Chapter 4.2.4 --- "1,1 -diphenyl-2-picrylhydrazyl (DPPH) Radical Scavenging Capacity" --- p.P.96 / Chapter 4.2.5 --- Primary Culture of Rat Aortic Endothelial Cells V --- p.P.96 / Chapter 4.2.6 --- Measurement Intracellular Oxidative Stress --- p.P.97 / Chapter 4.2.7 --- Nitric Oxide (NO) Measurement --- p.P.97 / Chapter 4.2.8 --- Drugs --- p.P.98 / Chapter 4.2.9 --- Data Analysis --- p.P.99 / Chapter 4.3 --- Results / Chapter 4.3.1 --- Impairment of Endothelium-dependent Relaxation by HC was Reversed by ROS Scavenger --- p.P.100 / Chapter 4.3.2 --- Brassicasterol Reversed HC-induced Endothelial Dysfunction In a Dose-dependent Manner --- p.P.102 / Chapter 4.3.3 --- β-Sitosterol and Stigmasterol Reversed HC-induced Endothelial Dysfunction --- p.P.104 / Chapter 4.3.4 --- Effects of β-Sitosterol Oxidation Products (SOPs) on HC-induced Endothelial Dysfunction --- p.P.106 / Chapter 4.3.5 --- Effects of Brassicasterol and β-Sitosterol on H2O2-induced Impairment of Endothelium-dependent Relaxation --- p.P.108 / Chapter 4.3.6 --- Phytosterols did not Directly Scavenge Free Radicals --- p.P.110 / Chapter 4.3.7 --- "HC and Brassicasterol did not Affect the Expression of SOD-1, SOD-2, eNOS, COX-1 and COX-2 in Aorta" --- p.P.112 / Chapter 4.3.8 --- HC Increased ROS Production in Primary Rat Aortic Endotelial Cells --- p.P.116 / Chapter 4.3.9 --- Brassicasterol did not Reverse the ROS Production by HC treatment In the Endothelial Cells --- p.P.120 / Chapter 4.3.10 --- Effect of L-NAME on Reversing the Effect of Brassicasterol on ACh-induced Relaxation --- p.P.123 / Chapter 4.3.11 --- Brassicasterol Reversed the Inhibitory Effect of HC on ACh-induced NO Production in Endothelial Cells --- p.P.125 / Chapter 4.4 --- Discussion --- p.P.128 / Chapter 4.5 --- Conclusion and Future Work --- p.P.132 / Chapter CHAPTER FIVE: --- CONCLUSIONS AND FUTURE WORK --- p.P.134 / Chapter CHAPTER SIX: --- REFERENCES --- p.P.137

Abstract not available

Bibliography: leaves 184-220.

Bibliography: leaves 140-190.

Object Rupture of intracranial arteriovenous malformations is a leading cause of stroke in children and young adults. Treatment options include surgery and highly focused radiation (stereotactic radiosurgery). For large and deep seated lesions, the risks of surgery may be prohibitively high, while radiosurgery has a disappointingly low efficacy and long latency. Radiosurgery carries the most promise for significant advances, however the process by which radiosurgery achieves obliteration is incompletely understood. Inflammation and thrombosis are likely to be important in the radiation response and may be amenable to pharmacological manipulation to improve radiosurgical efficacy. Materials and methods Immunohistochemistry and electron microscopy were used to study normal cerebral vessels, cavernous malformations and AVMs, some of which had previously been irradiated. An attempt was made to culture AVM endothelial cells to study the immediate response of AVM endothelium to radiosurgery. The effects of radiosurgery in a rat model of AVM were studied using immunohistochemistry and the results used to determine the choice of a pharmacological strategy to enhance the thrombotic effects of radiosurgery. Results Vascular malformations have a different endothelial inflammatory phenotype than normal cerebral vessels. Radiosurgery may cause long term changes in inflammatory molecule expression and leads to endothelial loss with exposure of pro-thrombotic molecules. Ultrastructural effects of irradiation include widespread cell loss, smooth muscle cell (SMC) proliferation and thrombosis. Endothelial culture from AVMs proved difficult due to SMC predominance in initial cultures. Radiosurgery upregulated several endothelial inflammatory molecules in the animal model and may induce pro-thrombotic cell membrane alterations. The administration of lipopolysaccharide and soluble tissue factor to rats following radiosurgery led to selective thrombosis of irradiated vessels. Conclusions Inflammation and thrombosis are important in the radiosurgical response of AVMs. Lumen obliteration appears to be mediated by proliferation of cells within the vessel wall and thrombosis. Upregulation of inflammatory molecules and perhaps disruption of the normal phospholipid asymmetry of the endothelial and SMC membranes are some of the earliest responses to radiosurgery. The alterations induced by radiation may be harnessed to selectively initiate thrombus formation. Stimulation of thrombosis may improve the efficacy of radiosurgery, increasing treatable lesion size and reducing latency.

Bibliography: leaves 140-190 / xiv, 190, [10] leaves : / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (M.D.)--University of Adelaide, 1987

People with diabetes are at a greater risk of burn injuries than those without diabetes. This stems from the epidemiological profiles of the conditions and the effects of morbidities associated with diabetes. Both conditions share some similarities in terms of metabolic alterations and suboptimal immune functions which may result in poor outcomes for patients. For that reason, it is reasonable to deduce that patients with diabetes are a challenging group to manage in burns units. However, this deduction should be taken cautiously because of lack of supporting evidence. Accordingly and after consulting with clinical experts, the research in this portfolio investigated the association between diabetes and burn injuries. In particular, two different aspects of this association were investigated in two individual quantitative and descriptive inquiries. The first was a case note review of patients hospitalised with a principal diagnosis of a foot burn injury in a large tertiary hospital in South Australia from 1999 to 2004. The second study investigated management of diabetes in burns units treating adults. This study is an e-mail survey of clinical leaders of burns units in Australia, New Zealand, Hong Kong and the United Kingdom. The clinical leaders were approached indirectly through key liaison persons in each identified unit. In the first study, outcomes for twelve subjects with and fifty-two without diabetes were described using descriptive and non-parametric statistics. In the second study, descriptive frequencies and content analysis were adopted to analyse twenty-nine responses from seventeen out of thirty burns units which participated in the study. Supporting findings in the literature, the first study showed that burn injuries among subjects with diabetes were mainly resulted from household devices. There were no statistically significant differences between subjects with and without diabetes in terms of size and depth of burn injuries and treatment received. In spite of this, there was a statistically significant association between diabetes and the experience of local post-burn complications and longer duration of hospitalisation. The second study indicated that more than twenty-five percent of the respondents believed that multidisciplinary centres should only occasionally be involved in the process of care. Participants reported that the individual profile of each patient plays a major role in determining the management of diabetes. Additionally, it was found that the insulin sliding scale was commonly used in the management of diabetes in burns units. The association between diabetes and a burn injury is a serious issue in terms of health and cost. This association need be addressed firstly and most importantly at the prevention level; secondly through proper management of both diabetes and burns. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1285462 / Thesis (D.Nurs.)--Population Health and Clinical Practice, 2007.

Common risk factors for CVD such as hyperlipidaemia, hypertriglyceridemia, low HDL-C, obesity, insulin resistance, impaired glucose tolerance, inflammation and hypertension may increase the risk of atherosclerosis through altering vascular function. Modification of dietary intake and weight loss can ameliorate these risk factors and may impede the development of atherosclerosis. CVD risk can be assessed by measurement of both traditional e.g. lipid levels, glucose and blood pressure and novel risk markers of CVD e.g. FMD, levels of adhesion molecules, inflammatory markers and adipokines. Changes in these measurements are used to determine effects, if any, of dietary interventions. The studies in this thesis focus on the relationship between nutrition and vascular function and the effects of modifying dietary composition either with, or without weight loss. The primary hypotheses addressed were that a high saturated fat diet would have adverse effects on markers of CVD risk., that short and long term weight loss would have beneficial effects on these markers, that a conventional low fat, high glycaemic load diet would also have adverse effects on these markers and that weight loss would attenuate the BP response to salt. Six studies were conducted to address these hypotheses. The effects of saturated fat were investigated in chapters 3 and 6. In chapter 3, a high saturated fat diet impaired FMD and increased the level of the adhesion molecule Pselectin compared with a high MUFA, a high PUFA, or a low fat, high glycaemic load diet in weight stability. The high fat, high glycaemic load caused increases of 23-39% in TG and decreases of 10-15% in HDL-C but despite these adverse effects there was no change in FMD. In chapter 6, subjects on a very low carbohydrate/high saturated fat diet lost approximately 1 kg more weight over 8 weeks than those on a conventional low fat diet. While other CVD risk factors, glucose, insulin, E and P-selectin, ICAM-1 and PAI-1 levels all improved FMD did not change in either diet. Reductions in LDL-C and CRP were greater on the conventional diet. The effects of weight loss on CVD risk factors were also investigated in the studies in chapters 4, 5, 7 & 8. In chapter 4, moderate weight loss using 2 different low fat diets resulted in improvements in PAI-1 and sICAM-1 but there was no change in FMD. Similarly in chapter 5 weight loss on a low carbohydrate/low saturated fat diet did not change FMD but there were other benefits including reductions in glucose and insulin, LDL-C, adhesion molecules, VCAM1 and ICAM1. Adiponectin did not change after short term weight loss in either of the studies in chapters 5 or 6. In chapter 7 salt loading increased ambulatory day time BP and this response was not altered by short term moderate weight loss. The long term effects of weight loss were investigated in chapters 5, 7 and 8. In chapter 5, after 52 weeks, there was sustained weight loss of 5% but no change in FMD while adiponectin levels increased and LDL-C and insulin were substantially reduced. In chapter 7 the BP response to salt loading remained unchanged despite weight loss maintenance. Finally in chapter 8 weight loss was predicted by protein intake and there were reductions in CVD risk demonstrated by decreases in insulin, TG and CRP and increases in HDL-C. The studies in this thesis demonstrate that moderate weight loss has beneficial effects on traditional and novel cardiovascular disease risk markers but does not have a beneficial effect on FMD regardless of dietary composition. A high saturated fat diet has detrimental effects on novel CVD risk markers in weight stability but weight loss attenuates this effect. A high saturated fat diet may have detrimental effects on adhesion molecules in weight stability and may attenuate the beneficial effects of weight loss on LDL-C and CRP. Moderate long term weight loss maintenance has beneficial effects on most but not all CVD risk markers. / http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1293779 / Thesis (Ph.D.) -- School of Medicine, 2007