This research explored the understanding of coronary heart disease among the South Asian Migrant men in the UK. The objectives of this study are: • To explore migrant South Asian men's understanding of the risks involved with coronary heart disease in the UK • To relate their understanding in the context of current health care policy • To suggest ways to provide culturally sensitive health promotion programs to these groups. A phenomenological perspective using qualitative research methodology and focus group interviews were used to obtain a more precise and in-depth understanding of the risks involved with coronary heart disease. In total 83 men were recruited. 13 focus groups were conducted in three different areas across the country which had a significant South Asian population. Three themes emerged from the analysis of the interviews: Psychosocial factor, conventional risk factors & health care experiences. These themes reflected the men's understanding of the risks Involved with coronary heart disease In the UK. According to Williams et al, (2007 & 2009), information about psychosocial risk profiles in UK South Asians is limited and that there is an increased possibility that psychosocial related factors contribute to increased vulnerability to coronary heart disease in South Asian in the UK. This study concludes with the importance of recognizing that not all South Asians are the same and that health professionals should look beyond the context of religious, and ethnic background and focus on individual men.

Please read the abstract in the section 00front of this document / Dissertation (MSc (Chemical Pathology))--University of Pretoria, 2005. / Chemical Pathology / unrestricted

京都大学 / 新制・課程博士 / 博士(工学) / 甲第23494号 / 工博第4906号 / 新制||工||1766(附属図書館) / 京都大学大学院工学研究科都市環境工学専攻 / (主査)教授 高野 裕久, 教授 米田 稔, 准教授 上田 佳代 / 学位規則第4条第1項該当 / Doctor of Philosophy (Engineering) / Kyoto University / DFAM

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Indiana University-Purdue University Indianapolis (IUPUI) / Risk of coronary artery disease (CAD), the leading cause of death, greatly increases in metabolic syndrome. Metabolic syndrome (MetS; obesity, insulin resistance, glucose intolerance, dyslipidemia, and hypertension) is increasing in prevalence with sedentary lifestyles and poor nutrition. Non-alcoholic steatohepatitis (NASH; i.e. MetS liver) is progressive and decreases life expectancy, with CAD as the leading cause of death. Pathogenic Ca2+ regulation transforms coronary artery smooth muscle from a healthy, quiescent state to a diseased, proliferative phenotype thus majorly contributing to the development of CAD. In particular, store-operated Ca2+ entry (SOCE) in vascular smooth muscle is associated with atherosclerosis. Genetic predisposition may render individuals more susceptible to Ca2+ dysregulation, CAD, NASH, and MetS. However, the metabolic and cellular mechanisms underlying these disease states are poorly understood. Accordingly, the goal of this dissertation was to investigate the role of dyslipidemia within MetS in the development of Ca2+ dysregulation, CAD, and NASH. The overarching hypothesis was that dyslipidemia within MetS would be necessary for induction of NASH and increased SOCE that would primarily mediate development of CAD. To test this hypothesis we utilized the Ossabaw miniature swine model of MetS. Swine were fed one of five diets for different lengths of time to induce varying severity of MetS. Lean swine were fed normal maintenance chow diet. F/MetS swine were fed high Fructose (20% kcal) diet that induced normolipidemic MetS. TMetS were fed excess high Trans-fat/cholesterol atherogenic diet that induced mildly dyslipidemic MetS and CAD. XMetS were TMetS swine with eXercise. DMetS (TMetS + high fructose) were moderately dyslipidemic and developed MetS and extensive CAD. sDMetS (Short-term DMetS) developed MetS with mild dyslipidemia, but no CAD. MMetS (Mixed-source-fat/cholesterol/fructose) were severely dyslipidemic, exhibited NASH, and developed severe CAD. Dyslipidemia in MetS predicted NASH severity (all groups < DMetS << MMetS), CAD severity (i.e. Lean, F/MetS, sDMetS < XMetS < TMetS < DMetS < MMetS), and was necessary for STIM1/TRPC1-mediated SOCE, which preceded CAD. Exercise ameliorated SOCE and CAD compared to TMetS. In conclusion, dyslipidemia elicits TRPC1/STIM1 SOCE that mediates CAD, is necessary for and predictive of NASH and CAD, and whose affects are attenuated by exercise.

Carotid artery wall stiffness has been widely considered as an index of vascular health, and has been associated with occurrence of cardiovascular events, such as stroke. In addition, the blood flow patterns in the carotid artery can yield crucial information on atherosclerosis progression and cerebrovascular impairment. Pulse wave imaging (PWI) is a non-invasive ultrasound imaging technique that tracks the propagation of the arterial pulse wave, providing thus regional arterial wall stiffness mapping. Moreover, towards enabling accurate visualization of blood flow patterns, ultrasound-based vector flow imaging (VFI) modalities have been developed. Building upon PWI and VFI techniques, the overall goal of this dissertation is to develop ultrasound-based methodologies that can provide simultaneous imaging of the carotid artery wall mechanics and blood flow dynamics at high temporal and spatial resolutions. The developed techniques are validated through vessel phantom experiments and simulations. Furthermore, their potential to diagnose pre-clinical stages of carotid artery disease and provide additional insights in risk for stroke assessment, is demonstrated in an atherosclerotic swine study and human subjects in vivo. More specifically: A method is presented that analyzes the pattern of arterial wall motion derived by PWI, in order to detect spatial mechanical inhomogeneity across an imaged artery, and provide piecewise arterial wall stiffness estimates. The proposed technique is validated in a phantom consisting of a soft and a stiff segment, while its feasibility is demonstrated to identify inhomogeneous wall properties in atherosclerotic human carotid arteries, as well as provide atherosclerotic plaque mechanical characterization in vivo. Subsequently, PWI is integrated with VFI techniques in the same ultrasound acquisition sequence, in order to enable simultaneous and co-localized imaging of arterial wall stiffness and blood vector flow velocity. The performance of the technique is investigated through experiments and FSI simulations. Moreover, its feasibility was shown to investigate associations between carotid artery Pulse Wave Velocity and blood flow patterns, in vivo. Based on the previously developed PWI and VFI modalities, a novel ultrasound-based technique is developed that combines high frame rate vector flow imaging with a data clustering approach, in order to enable direct and robust wall shear stress measurements. The performance of the proposed method is evaluated through vessel phantom experiments and simulations, while its feasibility is shown to detect pre-clinical stages of carotid artery disease in a swine model in vivo. In addition, a pilot clinical study is presented involving application of the developed modality in normal and atherosclerotic human carotid arteries in-vivo. Moving forward, the developed imaging modalities are used to implement novel clinical biomarkers based on carotid artery arterial wall mechanics and blood flow dynamics, that can potentially assist in risk for stroke assessment. The patterns of those biomarkers are investigated in the common carotid arteries of subjects with low degree of stenosis and medical history of stroke, against subjects without history of stroke. The same biomarkers are also analyzed with respect to stroke symptomatology in atherosclerotic patients with moderate to high degree of stenosis. Moreover, the developed techniques are used to identify vulnerable plaque components in subjects with fully developed plaques, as compared with CTA scans. Finally, a deep learning-based approach for motion tracking of the arterial wall throughout the cardiac cycle is proposed. A neural network is trained to learn the motion patterns of the carotid artery and potentially improve the quality of PWI. The performance of the technique is assessed in vessel phantom experiments and its feasibility is demonstrated in healthy human carotid arteries in-vivo.

This study aimed to i) investigate the prevalence of unhealthy attributes, common diseases, and inequities in social determinants of health across a large and representative sample of adults in New York City; and ii) identify common key predictors of COVID-19 seropositivity by comparing various regression models using a hierarchical regression method among a sample of New York City adults. The study will use the New York City Community Health Survey (NYC CHS) 2020 dataset for this analysis. An exploratory approach is used to data to understand the social, environmental, and individual determinants of health in the New York City population at the peak of the pandemic and their effects on COVID-19 seropositivity. The study also emphasizes on using a predictive modeling approach to develop and select an optimal ML model that accurately predicts COVID-19 seropositivity from various ML algorithms. Hierarchical logistic regression was carried out on a sample of 928 participants. It was found that age group 65-75, Black and Hispanic race and being born in the US were statistically significant factors in model 1 of the hierarchical regression where only socioeconomic factors were considered. With the inclusion of health behaviors, tobacco smoking behaviors, and physical activity were statistically significant. In the full model, BMI, asthma prevalence, and suicidal thoughts were statistically significantly correlated with COVID-19 seropositivity. The findings are consistent with public health literature highlighting the importance of healthy behaviors and public health efforts in maintaining overall health and immunity.

by Choi Ka Yan. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 113-128). / Abstract and appendix in English and Chinese. / Acknowledgements --- p.i / Abstract --- p.ii / Abstract (Chinese version) --- p.iv / Table of Contents --- p.vi / List of Tables --- p.xi / List of Figures --- p.xiv / List of Abbreviations --- p.xv / Chapter CHAPTER ONE: --- BACKGROUND AND LITERATURE REVIEW / Chapter 1.1 --- Coronary Heart Disease: a global health problem --- p.1 / Chapter 1.2 --- Risk Factors of Coronary Heart Disease --- p.3 / Chapter 1.2.1 --- Age --- p.3 / Chapter 1.2.2 --- Gender --- p.4 / Chapter 1.2.3 --- Family History of Cardiovascular Disease --- p.5 / Chapter 1.2.4 --- Hypercholesterolemia --- p.7 / Chapter 1.2.5 --- Unhealthy Dietary Habits --- p.11 / Chapter 1.2.6 --- Obesity --- p.14 / Chapter 1.2.7 --- Physical Inactivity --- p.20 / Chapter 1.3 --- Clustering of Risk Factors --- p.24 / Chapter 1.4 --- Risk Factors in Children: Atherosclerosis Begins Early in Life --- p.26 / Chapter CHAPTER TWO: --- RESEARCH IN HONG KONG AND PURPOSES OF THIS STUDY / Chapter 2.1 --- Nutrition Transition --- p.27 / Chapter 2.2 --- CHD Mortality Trends in Hong Kong --- p.28 / Chapter 2.3 --- Serum Total Cholesterol and Obesity in Hong Kong Adults --- p.29 / Chapter 2.4 --- "Obesity, Serum Total Cholesterol, Dietary Habits and Physical Activity of Hong Kong Children and Adolescents" --- p.31 / Chapter 2.5 --- Study Purpose and Objectives --- p.35 / Chapter CHAPTER THREE: --- SURVEY DESIGN / Chapter 3.1 --- Sample Selection --- p.39 / Chapter 3.2 --- "Blood Total Blood Cholesterol, Triglyceride and Anthropometric Measurements" --- p.40 / Chapter 3.2.1 --- Total Blood Cholesterol and Triglyceride --- p.40 / Chapter 3.2.2 --- Anthropometry Measures --- p.42 / Chapter 3.3 --- Questionnaire --- p.45 / Chapter 3.3.1 --- Questionnaire Design and Pre-testing --- p.45 / Chapter 3.3.2 --- General Health and Socio-demographic Questionnaire --- p.47 / Chapter 3.3.3 --- Physical Activity Questionnaire --- p.47 / Chapter 3.3.4 --- Dietary Questionnaire --- p.48 / Chapter 3.4 --- Data Management --- p.49 / Chapter 3.5 --- Statistics --- p.49 / Chapter 3.6 --- Data Analysis --- p.50 / Chapter 3.6.1 --- Blood Total Cholesterol and Triglyceride --- p.50 / Chapter 3.6.2 --- Obesity and Fat Distribution --- p.50 / Chapter 3.6.3 --- Diet --- p.51 / Chapter 3.6.4 --- Physical Activity Patterns --- p.51 / Chapter 3.6.5 --- Body Mass Index of Parent and Family History of Diseases --- p.52 / Chapter CHAPTER FOUR: --- RESULTS / Chapter 4.1 --- Sample Size and the Characteristics of the Students in the Two Schools --- p.54 / Chapter 4.2 --- Gender and Age Distribution --- p.55 / Chapter 4.3 --- Blood Total Cholesterol and Triglyceride --- p.56 / Chapter 4.4 --- Anthropometry Measures --- p.58 / Chapter 4.5 --- Dietary Habits --- p.60 / Chapter 4.5.1 --- Dietary Composition of 3-day Dietary Record --- p.60 / Chapter 4.5.2 --- Eating Behaviors --- p.65 / Chapter 4.6 --- Physical Activity --- p.68 / Chapter 4.7 --- Family History of Diseases --- p.70 / Chapter 4.8 --- Parents' Anthropometry --- p.71 / Chapter 4.9 --- Demographic Data --- p.71 / Chapter 4.10 --- Inter-relationships --- p.75 / Chapter 4.10.1 --- Blood Total Cholesterol and Triglyceride --- p.75 / Chapter a. --- "Blood Total Cholesterol, Triglyceride and Body Fatness" --- p.75 / Chapter b. --- "Blood Total Cholesterol, Triglyceride and Diet" --- p.75 / Chapter c. --- "Blood Total Cholesterol, Triglyceride and Physical Activity Patterns" --- p.77 / Chapter d. --- Blood Total Cholesterol，Triglyceride and Family History of Hypercholesterolemia --- p.78 / Chapter e. --- Relative Importance of the Key Factors in Predicting Blood Total Cholesterol levels --- p.79 / Chapter 4.10.2 --- Obesity and Body Fatness --- p.79 / Chapter a. --- "Obesity, Body Fatness and Physical Activity Patterns" --- p.79 / Chapter b. --- "Obesity, Body Fatness and Diets" --- p.82 / Chapter c. --- Body Fatness and Genetics --- p.84 / Chapter 4.10.3 --- Diet and Physical Activity --- p.86 / Chapter 4.10.4 --- "Blood Total Cholesterol, Triglyceride, Obesity and Other Demographic or Economic Characteristics" --- p.87 / Chapter 4.11 --- Clustering of Risk Factors among Obese children --- p.87 / Chapter CHAPTER FIVE: --- DISCUSSION / Chapter 5.1 --- Implication of Research Findings --- p.89 / Chapter 5.2 --- Limitations --- p.108 / Chapter CHAPTER SIX: --- CONCLUSIONS AND RECOMMENDATIONS --- p.111 / References --- p.113 / Appendices / Chapter I --- Questionnaire (English version) --- p.129 / Chapter II --- Questionnaire (Chinese version) --- p.139 / Chapter III --- Introductory letter (English version) --- p.152 / Chapter V --- Introductory letter (Chinese version) --- p.153 / Chapter V --- Consent form (English version) --- p.154 / Chapter VI --- Consent form (Chinese version) --- p.155 / Chapter VII --- Photos of the standard household measures given to children for estimation of portion size (English version) --- p.156 / Chapter VIII --- Photos of the standard household measures given to children for estimation of portion size (Chinese version) --- p.157 / Chapter IX --- Responses from the children to the food frequency questionnaire --- p.158 / Chapter X --- The frequency of the reported food items liked or disliked by the children --- p.160

The purpose of this study was to examine the role of anger/hostility on physiological and behavioral coronary heart disease risk factors. It was hypothesized that anger/hostility would contribute to the severity of CHD via consummatory behaviors such as smoking, poor diet, and excessive alcohol consumption. Some researchers suggest that negative consummatory behaviors play a direct causal role in CHD. The present study proposed that hostility predisposes an individual to these behaviors, and that these behaviors in turn, contribute to CHD. Further, it was proposed that some of the anger that exists in CHD patients may result from the individual being unable to participate in some of their previous consummatory behaviors after suffering a myocardial infarction. Also, it was hypothesized that the construct of anger/hostility would be differentially related to consummatory behaviors.