No description available.

No / The objective of this article was to evaluate the effectiveness of pharmacist-led medication review in chronic pain management. Six electronic databases (Medline, Embase, PsycInfo, CINHAL, CENTRAL, International Pharmaceutical Abstracts) reference lists of retrieved articles and relevant websites were searched for randomized controlled trials published in the English language involving adults with chronic pain. Studies were included if one of the intervention arms had received pharmacist-led medication review independently or as part of a multidisciplinary intervention. Risk of bias was assessed for all the included studies. The search strategy yielded 583 unique articles including 5 randomized controlled trials. Compared with control, meta-analysis showed that participants in the intervention group had: a 0.8-point reduction in pain intensity on a 0 to 10 numerical rating scale at 3 months [95% confidence interval (CI), -1.28 to -0.36] and a 0.7-point reduction (95% CI, -1.19 to -0.20) at 6 months; a 4.84 point (95% CI, -7.38 to -2.29) and -3.82 point (95% CI, -6.49 to -1.14) improvement in physical functioning on a 0- to 68-point function subscale of Western Ontario and McMaster Universities Osteoarthritis Index at 3 and 6 months, respectively; and a significant improvement in patient satisfaction equivalent to a "small to moderate effect." Pharmacist-led medication review reduces pain intensity and improves physical functioning and patient satisfaction. However, the clinical significance of these findings remain uncertain due to small effect size and nature of reported data within clinical trials that limits recommendation of wider clinical role of pharmacist in chronic pain management.

AIM: To evaluate marginal bone loss around dental implants at the 2nd stage abutment surgery and retrospectively evaluate the association of pre-surgical variables. MATERIAL AND METHODS: Eighty-seven subjects (41 Males and 46 females) were enrolled in this cohort. The subjects' ages ranged from 23 to 80 years. Two endosseous implant brands were utilized: Nobel Biocare and Straumann Bone Level . Clinical measurements (mesial, distal, buccal, and lingual) were recorded from the coronal margin of the implant platform to the bone margin with a periodontal probe (Williams periodontal probe, Hu-Friedy) at the time of implant placement and at the 2nd stage abutment surgery. The pre-surgical variables (medication intake, implant site, bone graft volume, membrane type, and smoking) were evaluated using Chi-square test. RESULTS: The marginal bone loss (MBL) difference was calculated. The Mean clinical MBL: Mesial = 0.71 mm, Distal = 0.56mm, Buccal/Labial = 0.65 mm, and Lingual/Palatal = 0.56 mm. The test showed no statistically significant difference between test and control subjects in each of the variables, with the exception of thyroid medication. A statistically significant (P value = 0.011) association was found between levothyroxine and MBL at the mesial measurement. CONCLUSION: This limited cohort study suggests that medication-controlled hypothyroidism patients may experience an increased risk of marginal alveolar bone loss around dental implants at the 2nd stage abutment surgery. The final determination will be recalculated when the study population reaches the estimated requirement of 200 subjects.

A Doença de Alzheimer é uma doença neurodegenerativa progressiva e de início tardio, que compromete principalmente as areas da cognição, julgamento e estabilidade emocional. Esta doença se caracteriza por dois tipos de lesões cerebrais características: emaranhados neurofibrilares e placas senis. Os emaranhados neurofibrilares são compostos por uma proteína do citoesqueleto (proteína tau) hiperfosforilada e agregada. As placas senis são formadas por agregados da proteína β-amilóide. A doença de Alzheimer é resultado dainteração de vários fatores ainda incompletamente elucidados; não obstante, o estresse oxidativo e os processos inflamatórios ocupam posição de destaque dentre esses fatores. Neste trabalho, avaliamos as atividades das enzimas eritrocitárias superóxido dismutase, catalase e glutationa peroxidase, assim como o conteúdo plasmático de glutationa total, vitamina C, α-tocoferol, β-caroteno, licopeno e coenzima Q10. A esses parâmetros antioxidantes foram contrapostas medidas de oxidação de lipídios e proteínas plasmáticas. Adicionalmente, efetuamos a avaliação das expressões monocitárias de HLADR e CD-11b, e das citocinas IL-6, IL-1α e TNF-α. Nossos resultados mostram que os pacientes de doença de Alzheimer possuem níveis circulantes de atocoferol inferiores aos pacientes controles, e possuem monócitos que apresentam maior expressão basal de HLA-DR e maior produção de IL-1α quando estimulados por LPS. Esses resultados fortalecem a hipótese inflamatória na doença de Alzheimer, de acordo com trabalhos recentes que apontam bons resultados com o a-tocoferol na sua prevenção e tratamento. / Alzheimer\'s disease is a late-onset, progressive degenerative disease that affects mainly the judgement, emotional stability and memory domains. This disease is characterized by two telltale cerebral lesions: neurofibrillary tangles and senile plaques. Neurofibrillary tangles are constituted by hyperphosphorylated cytoskeleton protein tau aggregates, while senile plaques are mainly composed by β-amyloid protein aggregates. Alzheimer\'s disease is the outcome of a complex interaction among several factors which are not fully understood yet; nevertheless it is clear thar oxidative stress and inflammatory pathways rate high among these factors. In this work, we evaluated the erythrocytic acitivities of superoxide dismutase, catalase and glutathione peroxidase, as well as the plasma levels of total glutathione, α-tocopherol, α-carotene, lycopene, and coenzyme Q10. These antioxidant parameters were confronted with plasmatic levels of protein and lipid oxidation products. Additionally, we measured the basal expression of monocyte HLA-DR and CD-11b, as well as the monocyte production of the cytokines IL1-α, IL-6 and TNF-α. Our results show that Alzheimer\'s Disease patients show lower plasmatic levels of α-tocopherol when compared to control patients, and have higher basal monocyte HLA-DR expression associated with higher IL-1α production when stimulated by LPS. These results lend support to the inflammatory theory of Alzheimer\'s disease, according to recent works that indicate good results of α-tocopherol administration in both its prevention and treatment.

Introdução: A formação de atelectasia durante a indução anestésica pode ser um dos fatores responsáveis pela ocorrência de complicações pulmonares pós-operatórias (CPP). A aplicação de pressão positiva expiratória ao final da expiração (PEEP), uso criterioso de altas frações inspiradas de oxigênio e a utilização de manobras de recrutamento alveolar no período intra-operatório são recursos utilizados para a prevenção de atelectasia em procedimentos anestésicos. O objetivo deste estudo foi avaliar o modelo de ventilação mecânica adotado em procedimentos anestésicos de longa duração e suas correlações com as complicações pulmonares pós-operatórias. Métodos: Foram avaliadas em estudo observacional as cirurgias com mais de cinco horas de duração. No início do procedimento anestésico, na sala de cirurgia e após o seu término, na unidade de terapia intensiva, os parâmetros ventilatórios utilizados foram anotados e correlacionados com os achados das radiografias torácicas e saturação periférica de oxigênio (SpO2) em ar ambiente. Resultados: Cento e vinte e um pacientes foram observados. O tempo total de anestesia 499,4 ± 159,8 minutos. O volume corrente (VC) determinado no período intraoperatório foi 8,09 ± 2,15 mL/kg e a PEEP utilizada de 3,05 ± 2,31 cmH2O. Houve diferença para a mediana da SpO2 em ar ambiente (96% [95-97] vs 95% [92-96], p <0,001) comparando os períodos pré e pós-operatório. A freqüência de pacientes que apresentaram atelectasia nas radiografias de tórax do período pós-operatório (38,8%) foi significantemente maior que a do período pré-operatório (0%), x2=32,259. Não foi encontrado correlação entre os achados e o tempo de anestesia (p=0,708); a PEEP intra-operatória (p=0,296); tempo de permanência com suporte ventilatório mecânico no pósoperatório (p = 0,146) e tabagismo (p = 0,563). Conclusões: No período intra-operatório o PEEP utilizado em procedimentos de longa duração é baixo. Ocorre queda na SpO2 e aumento na incidência de atelectasia no período pós-operatório em comparação com o pré-operatório. São necessários outros estudos para melhor avaliação dos fatores responsáveis / Introduction: The formation of the atelectasis during the induction of the anesthesia can be one of the factors involved in the occurrence of postoperative pulmonary complications (PPCs). The application of the positive end-expiratory pressure (PEEP), low inpiratory concentrations of oxygen and the alveolar recruitment maneuvers perform in the intraoperative period are approaches used in the prevention of atelectasis in the anesthesia procedures. The objective of this study was to evaluate, in prospective observational study, the pattern of mechanical ventilatory assistence during longer anesthesia procedures and its correlations with the PPCs. Methods: The surgeries procedures longer than five hours have been evaluated in observational study. At the beginning of the anesthesia procedure, in the operatory room and after its terminus, in the intensive care unit, the mechanical ventilation parameters were determined and correlated with the findings in the chest x-rays and peripheral oxygen saturation (SpO2) in room air. Results: One hundred twenty one patients have been observed. The total time of anesthesia was 499,4 ± 159,8 minutes. The tidal volume (VT) in the intraoperative period was 8,09 ± 2,15 mL/kg and the PEEP used was 3,05 ± 2,31 cmH2O. There was a difference for the median of the SpO2 in room air (96% [95-97] vs 95% [92-96], p <0,001) comparing the pre and postoperative periods. The frequency of patients who had presented atelectasis in the chest x-rays of the postoperative period (38,8%) was significantly higher than the preoperative period (0%), x2=32,259. No correlation was found among these findings and the anesthesia time (p=0,708); the intraoperative PEEP used (p=0,296); time with mechanical ventilatory support in the postoperative period (p = 0,146) and smoking habits (p = 0,563). Conclusions: In the intraoperative period, the PEEP is low in longer procedures. The SpO2 decreases and the incidence of the atelectasis increases in the postoperative period, when compared with the preoperative one. Other researches are required for better evaluation of the factors related for the development of the PPCs

A metionina sintase redutase (MTRR) catalisa a redução da cobalamina (Cbl) oxidada a metilcobalamina. Em presença de folato, a metionina sintase (MTR) utiliza a metilcobalamina como cofator na metilação da homocisteína (tHcy) a metionina. O objetivo deste estudo foi avaliar os efeitos dos polimorfismos MTR A2756G e MTRR A66G nas concentrações dos metabólitos marcadores de deficiência de Cbl e folato em gestantes e neonatos. Os genótipos dos polimorfismos MTR A2756G e MTRR A66G foram obtidos por PCR-RFLP. O genótipo MTR 2756AA foi relacionado aos maiores valores de tHcy em gestantes e MMA em neonatos. Gestantes com genótipos MTRR 66AG e GG e com menores concentrações de Cbl apresentaram maior risco de apresentar concentrações elevadas de tHcy. Neonatos com genótipos com MTRR 66AG e GG apresentaram menores valores de SAM. Os polimorfismos MTR A2756G e MTRR A66G interferem nas reações dependentes de Cbl e folato em gestantes e neonatos. / Methionine synthase reductase (MTRR) catalyzes the reductive reaction of oxidized cobalamin to methylcobalamin. When folate is present, methionine synthase (MTR) uses methylcobalamin cofactor at homocysteine to methionine methylation process. The aim of this study was to evaluate the effects of MTR A2756G and MTRR A66G polymorphisms on total homocysteine (tHcy), methylmalonic acid (MMA), S-adenosylmethionine (SAM) concentrations and SAM/SAH ratio in Brazilian pregnant women and their newborns. Genotypes of two polymorphisms were determined by PCR-RFLP. MTR 2756AA genotype was associated with higher tHcy and MMA levels in mothers and babies, respectivelly. Lower cobalamin concentrations associated with MTRR 66AG and GG genotypes increased risk to elevated tHcy levels in pregnant women. The SAM levels were lower in neonates with MTRR 66AG e GG genotypes. The polymorphisms MTR A2756G and MTRR A66G could affect cobalamin and folate dependent reactions in pregnant women and newborns.

Fung, Kit Ching. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 134-144). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese. / Some appendixes in Chinese.

Lau Wing-Ngar Vivian. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2002. / Includes bibliographical references (leaves 135-144). / Abstracts in English and Chinese. / Acknowledgements --- p.i / Abstract --- p.ii / Abbreviations --- p.vi / List of figures --- p.viii / List of tables --- p.xi / Contents --- p.xiii / Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- General introduction --- p.1 / Chapter 1.2 --- Roadside air pollution worldwide and in Hong Kong --- p.2 / Chapter 1.2.1 --- Air quality in Hong Kong --- p.3 / Chapter 1.3 --- Characteristics of particulate matter --- p.9 / Chapter 1.4 --- Composition and sources of particulate matter --- p.11 / Chapter 1.5 --- Toxic effects of particulate matter --- p.12 / Chapter 1.5.1 --- Lung injury --- p.12 / Chapter 1.5.2 --- Cardiovascular injury --- p.15 / Chapter 1.5.3 --- Mutagenesis and carcinogenesis --- p.16 / Chapter 1.6 --- Aims of my study --- p.16 / Chapter 2 --- Toxic Effects of Heavy Metals Ions on Selected Cultured Cell-lines --- p.18 / Chapter 2.1 --- Introduction --- p.18 / Chapter 2.1.1 --- Metals --- p.18 / Chapter 2.1.1.1 --- Cadmium --- p.22 / Chapter 2.1.1.2 --- Chromium --- p.23 / Chapter 2.1.1.3 --- Lead --- p.25 / Chapter 2.1.1.4 --- Zinc --- p.26 / Chapter 2.1.2 --- Metallothioneins --- p.28 / Chapter 2.1.3 --- p53 --- p.31 / Chapter 2.1.4 --- Tumor Necrosis Factor-alpha (TNF-α) --- p.32 / Chapter 2.1.5 --- Aims of this chapter --- p.32 / Chapter 2.2 --- Materials and methods --- p.35 / Chapter 2.2.1 --- Reagents --- p.35 / Chapter 2.2.2 --- Cultured Cell lines --- p.35 / Chapter 2.2.2.1 --- PU5-18 --- p.36 / Chapter 2.2.2.2 --- LL24 --- p.36 / Chapter 2.2.2.3 --- HBE4-E6/E7 --- p.37 / Chapter 2.2.3 --- Cytotoxicity assays --- p.37 / Chapter 2.2.4 --- ELISA assays --- p.40 / Chapter 2.2.4.1 --- ELISA assay ofp53 levels --- p.41 / Chapter 2.2.4.2 --- ELISA assay of TNF-α levels --- p.43 / Chapter 2.2.5 --- MT gene expression studies by Luciferase assay --- p.44 / Chapter 2.2.5.1 --- PCR amplification --- p.44 / Chapter 2.2.5.2 --- 5´ة End modification of PCR amplified DNA --- p.44 / Chapter 2.2.5.3 --- Ligation of DNA fragment to linearized vector --- p.46 / Chapter 2.2.5.4 --- E. coli. transformation by heat shock --- p.46 / Chapter 2.2.5.5 --- PCR sequencing --- p.47 / Chapter 2.2.5.6 --- Transfection of plasmid into HBE4-E6/E7 cells --- p.49 / Chapter 2.2.5.7 --- Data analysis --- p.50 / Chapter 2.3 --- Results and discussion --- p.51 / Chapter 2.3.1 --- Cytotoxicity assays --- p.51 / Chapter 2.3.2 --- Combination effects of metals on cytotoxicity --- p.61 / Chapter 2.3.3 --- p53 --- p.65 / Chapter 2.3.4 --- TNF-α --- p.68 / Chapter 2.3.5 --- MT gene expression studies by Luciferase assay --- p.69 / Chapter 2.4 --- Conclusion --- p.74 / Chapter 3 --- Effects of Polycyclic Aromatic Hydrocarbons (PAHs) on Cultured Cell-lines --- p.75 / Chapter 3.1 --- Introduction --- p.75 / Chapter 3.2 --- Materials and methods --- p.79 / Chapter 3.2.1 --- Reagents --- p.79 / Chapter 3.2.2 --- Cell culture --- p.79 / Chapter 3.2.3 --- AlamarBlue assay --- p.80 / Chapter 3.2.4 --- EROD assay --- p.80 / Chapter 3.3 --- Results and discussion --- p.84 / Chapter 3.4 --- Conclusion --- p.88 / Chapter 4 --- Chemical and Biological Assays on Roadside Dust --- p.89 / Chapter 4.1 --- Introduction --- p.89 / Chapter 4.1.1 --- Composition of particulate matter in Hong Kong --- p.89 / Chapter 4.1.2 --- Metal contents of particulate matter in Hong Kong --- p.91 / Chapter 4.1.3 --- Possible adverse health impacts of particulate matter --- p.94 / Chapter 4.1.3.1 --- In vitro studies using different cell models --- p.94 / Chapter 4.1.3.2 --- In vivo studies using rodents --- p.97 / Chapter 4.1.3.3 --- Epidemiological studies --- p.98 / Chapter 4.1.4 --- Aims of this chapter --- p.100 / Chapter 4.2 --- Materials and methods --- p.101 / Chapter 4.2.1 --- Sampling of roadside dust --- p.101 / Chapter 4.2.2 --- Chemical analysis of roadside dust --- p.104 / Chapter 4.2.2.1 --- Reagents --- p.104 / Chapter 4.2.2.2 --- Total metal contents --- p.105 / Chapter 4.2.2.3 --- Extractable metal contents --- p.105 / Chapter 4.2.3 --- Biological assays --- p.105 / Chapter 4.2.3.1 --- Cell models --- p.106 / Chapter 4.2.3.2 --- Pretreatment of roadside dust --- p.106 / Chapter 4.2.3.3 --- AlamarBlue assay --- p.106 / Chapter 4.2.3.4 --- ELISA assays --- p.108 / Chapter 4.2.3.5 --- Luciferase assay --- p.108 / Chapter 4.3 --- Results and discussion --- p.110 / Chapter 4.3.1 --- Total metal contents --- p.110 / Chapter 4.3.2 --- Extractable metal contents --- p.113 / Chapter 4.3.3 --- AlamarBlue assay --- p.116 / Chapter 4.3.4 --- p53 --- p.122 / Chapter 4.3.5 --- TNF-α --- p.122 / Chapter 4.3.6 --- Luciferase assay --- p.126 / Chapter 4.4 --- Conclusion --- p.129 / Chapter 5 --- General discussion and conclusion --- p.130 / Chapter 6 --- References --- p.135

As infecções são a causa mais freqüente de morbidade e mortalidade observadas tanto aguda como tardiamente nos pacientes receptores de transplante pulmonar, o que pode estar diretamente relacionado a uma deficiência no transporte mucociliar do sistema respiratório. Nosso objetivo foi avaliar a influência de dois fatores envolvidos com o transplante pulmonar sobre o transporte mucociliar de ratos: a secção e anastomose brônquica e a imunossupressão pela ciclosporina A. Setenta e dois ratos foram distribuídos aleatoriamente em cinco grupos de acordo com: i) procedimento operatório e ii) terapia a que seriam submetidos. Os resultados mostram que houve uma diminuição significativa da Freqüência de Batimento Ciliar in situ, da Transportabilidade do Muco in vitro e da Velocidade de Transporte Mucociliar in situ medidos a partir do brônquio principal esquerdo dos ratos tratados com ciclosporina A (p<0,001). A Freqüência de Batimento Ciliar in situ dos brônquios operados mostrou-se diminuída também no grupo tratado com solução salina e sacrificado no 30º dia após a operação (p=0,001). Já a Velocidade de Transporte Mucociliar in situ mostrou uma diminuição significativa em todos os grupos submetidos à secção brônquica (p<0,001). Houve um efeito sinérgico entre a terapia com ciclosporina A e a secção brônquica, causando um prejuízo ao transporte mucociliar ainda maior do que quando analisados isoladamente. Concluímos que a Velocidade de Transporte Mucociliar in situ foi agudamente prejudicada após a secção brônquica e terapia imunossupressora pela ciclosporina A, havendo diminuição da freqüência de batimento dos cílios e alteração das propriedades viscoelásticas do muco respiratório. / Infections are the most common cause of early and late morbidity and mortality in lung transplant recipient, and can be directly related to impaired mucociliary transport. Our aim was to assess the influence of bronchial section and imunossupression on mucociliary transport in rats. Seventy two rats were randomly distributed in five groups according to i) surgical procedure and ii) drug therapy. There was a significant impairment on Ciliary Beating Frequency in situ, Mucus Transportability Rate in vitro and Mucociliary Transport Speed in situ from operated bronchus of cyclosporine A-treated rats (p<0.001). Ciliary Beating Frequency from operated bronchus was also impaired in saline-treated rats that were killed on 30th postoperative day (p=0.001). Mucociliary Transport Speed was impaired in all bronchi underwent to section (p<0.001). We conclude that bronchial section and cyclosporine therapy impaired all factors analyzed. Also there was a synergic effect between cyclosporine therapy and bronchial section on ciliary beating frequency.

Ng Chi Ho. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references (leaves 147-160). / Abstracts in English and Chinese. / ACKNOWLEDGMENTS --- p.I / ABSTRACT --- p.II / LIST OF ABBREVIATIONS --- p.VII / TABLE OF CONTENTS --- p.IX / Chapter CHAPTER 1 --- GENERAL INTRODUCTION / Chapter 1.1 --- Introduction of Low-density lipoprotein --- p.1 / Chapter 1.1.1 --- What are lipids? --- p.1 / Chapter 1.1.2 --- Function and structure of cholesterol --- p.1 / Chapter 1.1.3 --- Function and classification of lipoprotein --- p.1 / Chapter 1.2 --- Functions of low-density lipoprotein --- p.2 / Chapter 1.3 --- Basic structure of low-density lipoprotein --- p.4 / Chapter 1.4 --- Principle on isolation and purification of low-density lipoprotein --- p.4 / Chapter 1.5 --- Cholesterol transport system --- p.7 / Chapter 1.5.1 --- Exogenous pathway of cholesterol metabolism --- p.7 / Chapter 1.5.2 --- Endogenous pathway of cholesterol metabolism --- p.7 / Chapter 1.5.3 --- Reverse transport of Cholesterol --- p.8 / Chapter 1.6 --- Oxidation of LDL --- p.10 / Chapter 1.6.1 --- Agents that causes oxidation --- p.10 / Chapter 1.6.1.1 --- Lipoxygenases --- p.10 / Chapter 1.6.1.2 --- Myeloperoxidase --- p.10 / Chapter 1.6.1.3 --- Reactive nitrogen species --- p.11 / Chapter 1.6.1.4 --- Reactive oxygen species --- p.11 / Chapter 1.6.2 --- Factors that affect the susceptibility of LDL oxidation --- p.13 / Chapter 1.7 --- Hyperlipidaemia 一 chance to increase LDL oxidation --- p.13 / Chapter 1.7.1 --- Definition of hyperlipidemia and hypercholesterolemia --- p.13 / Chapter 1.7.2 --- Risk factors of hyperlipidaemia --- p.13 / Chapter 1.7.2.1 --- High fat low fibre diets: --- p.13 / Chapter 1.7.2.2 --- Obesity --- p.14 / Chapter 1.7.2.3 --- Type II diabetes --- p.14 / Chapter 1.7.2.4 --- Genetic factors (Familial hyperlipidemias) --- p.14 / Chapter 1.8 --- Diseases related to oxidized LDL --- p.15 / Chapter 1.8.1 --- Cardiovascular diseases --- p.15 / Chapter 1.8.1.1 --- Atherosclerosis and ischemic heart attack --- p.15 / Chapter 1.8.1.2 --- Factors that affect incidence of atherosclerosis --- p.16 / Chapter 1.8.1.2.1 --- Triglyceride-rich lipoprotein --- p.16 / Chapter 1.8.1.2.2 --- Small and dense LDL --- p.16 / Chapter 1.8.1.3 --- Stroke --- p.17 / Chapter 1.8.2 --- Common ways to reduce plasma cholesterol level --- p.17 / Chapter 1.8.2.1 --- Diet control --- p.17 / Chapter 1.8.2.2 --- Physical activity --- p.17 / Chapter 1.8.2.3 --- Drug therapy --- p.18 / Chapter CHAPTER 2 --- IMPAIRMENT OF OXIDIZED LDL ON ENDOTHELIUM-DEPENDENT RELAXATION / Chapter 2.1 --- Introduction --- p.19 / Chapter 2.1.1 --- Properties and function of phenylephrine hydrochloride --- p.22 / Chapter 2.1.2 --- Properties and function of acetylcholine --- p.22 / Chapter 2.2 --- Objectives --- p.23 / Chapter 2.3 --- Materials and methods --- p.24 / Chapter 2.3.1 --- Preparation of drugs --- p.24 / Chapter 2.3.2 --- Preparation of human native LDL --- p.25 / Chapter 2.3.3 --- Preparation of oxidized LDL --- p.27 / Chapter 2.3.4 --- Preparation of aorta --- p.27 / Chapter 2.3.5 --- Measurement of Isometric Force in vitro --- p.30 / Chapter 2.3.5.1 --- Protocol 1- Dose effect of oxidized LDL on acetylcholine-induced vasorelaxation --- p.30 / Chapter 2.3.5.2 --- Protocol 2 - Time effect of oxidized LDL on acetylcholine-induced vasorelaxation --- p.30 / Chapter 2.3.5.3 --- Protocol 3 - Effect of co-incubation of LDL and copper(ll) sulphate on acetylcholine-induced vasorelaxation --- p.31 / Chapter 2.3.5.4 --- Protocol 4 - Effect of oxidized LDL on selected vasodilators --- p.32 / Chapter 2.3.5.5 --- Protocol 5 - Effect of pretreatment of L-arginine on oxidized LDL impaired -endothelium-induced relaxation --- p.32 / Chapter 2.3.5.6 --- Protocol 6 - Effect of a -tocopherol on oxidized LDL-damaged acetylcholine- induced vasorelaxation --- p.33 / Chapter 2.3.5.7 --- Protocol 7 - Effect of a -tocopherol on LDL and copper(ll) sulphate- induced endothelial dysfunction --- p.33 / Chapter 2.3.6 --- Western blot analysis of endothelial nitric oxide synthase (eNOS) protein --- p.34 / Chapter 2.3.7 --- Statistics --- p.35 / Chapter 2.4 --- Results --- p.36 / Chapter 2.4.1 --- Dose effect of oxidized LDL on acetylcholine-induced vasorelaxation --- p.36 / Chapter 2.4.2 --- Time effect of oxidized LDL on acetylcholine-induced vasorelaxation --- p.36 / Chapter 2.4.3 --- Effect of co-incubation of LDL and copper(II) sulphate on acetylcholine- induced vasorelaxation --- p.39 / Chapter 2.4.4 --- Effect of oxidized LDL on selected vasodilators --- p.41 / Chapter 2.4.5 --- Effect of pretreatment of L-arginine on oxidized LDL impaired- acetylcholine-induced relaxation --- p.41 / Chapter 2.4.6 --- Effect of a-tocopherol on oxidized LDL-damaged acetylcholine- induced vasorelaxation --- p.48 / Chapter 2.4.7 --- Effect of a-tocopherol on LDL and copper(II) sulphate-induced endothelial dysfunction --- p.50 / Chapter 2.4.8 --- eNOS Protein expression --- p.50 / Chapter 2.5 --- Discussion --- p.53 / Chapter CHAPTER 3 --- EFFECTS OF LDL INJECTION ON THE ENDOTHELIAL FUNCTION OF RATS / Chapter 3.1 --- Introduction --- p.58 / Chapter 3.2 --- Objective --- p.60 / Chapter 3.3 --- Methods and Materials --- p.61 / Chapter 3.3.1 --- Preparation of Drugs --- p.61 / Chapter 3.3.2 --- Preparation of LDL --- p.61 / Chapter 3.3.3 --- Animal Treatment --- p.61 / Chapter 3.3.4 --- Serum lipid and lipoprotein determinations --- p.62 / Chapter 3.3.5 --- Measurement of serum MDA level by TBARS assay --- p.62 / Chapter 3.3.6 --- Preparation of aorta --- p.62 / Chapter 3.3.7 --- Organ bath experiment --- p.63 / Chapter 3.3.8 --- Statistics --- p.64 / Chapter 3.4 --- Result --- p.65 / Chapter 3.4.1 --- Growth and food intake --- p.65 / Chapter 3.4.2 --- "Effect of LDL injection on serum TC, TG and HDL-C" --- p.65 / Chapter 3.4.3 --- Effect of LDL injection on non-HDL-C and ratio of non-HDL-C to HDL-C --- p.65 / Chapter 3.4.4 --- Serum MDA level --- p.68 / Chapter 3.4.5 --- Phenylephrine-induced contraction --- p.70 / Chapter 3.4.6 --- Endothelium-dependent and -independent relaxation --- p.75 / Chapter 3.5 --- Discussion --- p.79 / Chapter CHAPTER 4 --- EFFECTS OF INDIVIDUAL COMPONENT OF OXIDIZED LDL ON ENDOTHELIUM-DEPENDENT RELAXATION / Chapter 4.1 --- Introduction --- p.83 / Chapter 4.2 --- Objectives --- p.85 / Chapter 4.3 --- Materials and methods --- p.86 / Chapter 4.3.1 --- Preparation of drugs --- p.86 / Chapter 4.3.2 --- Preparation of human native LDL and oxidized LDL --- p.86 / Chapter 4.3.3 --- GC analysis of fatty acid composition in LDL --- p.86 / Chapter 4.3.4 --- TBARS assay analysis of MDA content in LDL --- p.87 / Chapter 4.3.5 --- GC analysis of cholesterol oxidation products in LDL --- p.89 / Chapter 4.3.6 --- Thin-layer chromatography analysis of LPC in LDL --- p.91 / Chapter 4.3.7 --- Preparation of aorta --- p.92 / Chapter 4.3.8 --- Measurement of Isometric Force in vitro --- p.92 / Chapter 4.3.8.1 --- Protocol 1- effect of LPC on acetylcholine-induced vasorelaxation --- p.92 / Chapter 4.3.8.2 --- Protocol 2- effect of cholesterol oxidation products on acetylcholine-induced vasorelaxation --- p.92 / Chapter 4.3.8.3 --- Protocol 3- effect of oxidized fatty acids on acetylcholine-induced vasorelaxation --- p.93 / Chapter 4.3.9 --- Statistics --- p.93 / Chapter 4.4 --- Results --- p.94 / Chapter 4.4.1 --- Compositional differences between native LDL and oxidized LDL.… --- p.94 / Chapter 4.4.2 --- Effect of LPC on endothelium-dependent relaxation --- p.98 / Chapter 4.4.3 --- Effect of COPs on endothelium-dependent relaxation --- p.98 / Chapter 4.4.4 --- Effect of oxidized fatty acids on endothelium-dependent relaxation --- p.101 / Chapter 4.5 --- Discussion --- p.103 / Chapter CHAPTER 5 --- EFFECTS OF DIETARY OXIDIZED CHOLESTEROL ON BLOOD CHOLESTEROL LEVEL IN HAMSTERS / Chapter 5.1 --- Introduction --- p.107 / Chapter 5.2 --- Objectives --- p.111 / Chapter 5.3 --- Materials and Methods --- p.112 / Chapter 5.3.1 --- Preparation of Oxidized Cholesterol --- p.112 / Chapter 5.3.2 --- Diet preparation --- p.112 / Chapter 5.3.3 --- Animals --- p.113 / Chapter 5.3.4 --- Serum lipid and lipoprotein determinations --- p.116 / Chapter 5.3.5 --- GC analysis of cholesterol and cholesterol oxidation products on organs --- p.116 / Chapter 5.3.6 --- Extraction of neutral and acidic sterols from fecal samples --- p.117 / Chapter 5.3.6.1 --- Determination of neutral sterols --- p.117 / Chapter 5.3.6.2 --- Determination of acidic sterols --- p.117 / Chapter 5.3.6.3 --- GLC analysis of neutral and acidic sterols --- p.118 / Chapter 5.3.7 --- Organ bath experiment --- p.121 / Chapter 5.3.7.1 --- Preparation of aorta --- p.121 / Chapter 5.3.7.2 --- Aortic relaxation --- p.121 / Chapter 5.3.8 --- Analysis of the total area of atherosclerotic plaque on aorta --- p.122 / Chapter 5.3.9 --- Statistics --- p.122 / Chapter 5.4 --- Results --- p.123 / Chapter 5.4.1 --- GC of oxidized cholesterol --- p.123 / Chapter 5.4.2 --- Growth and food intake --- p.123 / Chapter 5.4.3 --- "Effect of non-oxidized and oxidized cholesterol on serum TC, TG and HDL-C" --- p.123 / Chapter 5.4.4 --- Effect of non-oxidized and oxidized cholesterol on non-HDL-C and ratio of non-HDL-C to HDL-C --- p.124 / Chapter 5.4.5 --- Effect ofnon-oxidized and oxidized cholesterol on concentration of hepatic cholesterol --- p.128 / Chapter 5.4.6 --- Effect of non-oxidized and oxidized cholesterol on concentration of cholesterol oxidation products accumulated in liver --- p.128 / Chapter 5.4.7 --- Effect of non-oxidized and oxidized cholesterol on concentration of brain and aortic cholesterol --- p.128 / Chapter 5.4.8 --- Effect of non-oxidized and oxidized cholesterol on fecal neutral and acidic sterols --- p.129 / Chapter 5.4.9 --- Effect of non-oxidized and oxidized cholesterol on aortic relaxation --- p.135 / Chapter 5.4.10 --- Effect of non-oxidzied and oxidized cholesterol on area of atherosclerotic plaque --- p.137 / Chapter 5.5 --- Discussion --- p.139 / Chapter CHAPTER 6 --- CONCLUSION --- p.143 / REFERENCES --- p.146