Background: This dissertation comprises research conducted on two distinct projects. Project I focuses on the connection between household air pollution (HAP) from cooking with biomass fuels and blood pressure (BP); this research is situated in the context of a large randomized trial of a cookstove intervention in Ghana, West Africa. The setting of Project II, meanwhile, is the residential environment of New York City, where we explore temperature and humidity conditions in homes and relate these conditions to summertime heat wave risk and to the survival and transmission of respiratory viruses in the winter. Although these projects are quite distinct, each relates to the complex relationship between climate change and health. Reducing HAP to improve health (the focus of Project I) will simultaneously reduce climate change through a reduction in emissions of short-lived climate pollutants into the atmosphere. Meanwhile, furthering our understanding of heat and humidity levels inside urban residences (the focus of Project II) is crucial to our ability to protect health in light of projections for a changing climate. Domestic activities associated with heating, cooling, and cooking are thus very relevant both to human health and to climate change mitigation and adaptation. Objectives and Methods: Our overall objective for Project I was to investigate exposure- response relationships between HAP and BP in a cohort of pregnant women taking part in the Ghana Randomized Air Pollution and Health Study (GRAPHS). We first explored this association in a cross-sectional study (Chapter 1), in which we used 72-hour personal monitoring to ascertain levels of exposure among the GRAPHS women to carbon monoxide (CO), one of the pollutants emitted by traditional wood-fed cooking fires. These exposure data were collected at enrollment into the GRAPHS study, prior to the initiation of cooking with improved cookstoves. We investigated the association between these “baseline” CO exposure levels and the women’s blood pressure at enrollment into GRAPHS. A limitation of this study was that BP was only measured once. We followed this with a second study of 44 women drawn from the same cohort (Chapter 2), for whom we designed BP protocols using 24-hour ambulatory blood pressure monitoring (ABPM), the current gold standard for clinical diagnosis of hypertension. As we were not aware of any prior research in Africa that had employed ABPM, we also designed a parallel BP protocol using home blood pressure monitoring (HBPM) equipment for comparison with ABPM. The use of ABPM with concurrent personal CO monitoring enabled us to investigate hourly associations between CO exposure and changes in BP. We also evaluated BP in these women both before and after the cookstove intervention; this allowed us to investigate whether any changes in BP were associated with switching to an improved cookstove. Our objectives for Project II were to understand the distribution of temperature and humidity conditions in a range of New York City homes during the summer and winter seasons, to evaluate the impact of structural and behavioral factors (e.g. building size, use of air conditioning, and use of humidifiers) on these conditions, and to build models that could help predict indoor conditions from more readily available outdoor measurements. We conducted this research in two ways. We first analyzed a set of indoor temperature and humidity measurements that were collected in 285 New York City apartments during portions of summers 2003-2011 and used these data to simulate indoor conditions during two heat wave scenarios, one of which was more moderate and the other of which was more extreme (Chapter 3). Second, we designed and conducted a new study in which temperature and humidity were monitored in a set of 40 NYC apartments between 2013 and 2015 (Chapters 4-6). This second study enabled us extend our research into the winter season, and also to explore how factors such as air conditioning and humidifier use impacted indoor temperature and humidity. We also investigated relationships between the monitored conditions, self-reported perceptions of the indoor environment, and symptoms that were experienced among household members. Results: In the cross-sectional analysis of CO and BP in the GRAPHS cohort (Chapter 1), we found a significant positive association between CO exposure and diastolic blood pressure (DBP): on average, each 1 ppm increase in exposure to CO was associated with 0.43 mmHg higher DBP [0.01, 0.86]. A non-significant positive trend was also observed for systolic blood pressure (SBP). In our study of the acute relationship between CO exposure and BP (Chapter 2), we determined that peak CO exposure (defined as above the 90th percentile of the exposure distribution, or an average of 4.1ppm) in the two hours prior to BP measurement was associated with elevations in hourly systolic BP (4.3 mmHg [95% CI: 1.1, 7.4]) and diastolic BP (4.5 mmHg [95% CI: 1.9, 7.2]), as compared to BP following lower CO exposures. We also observed a non-significant trend toward lower BP following initiation of cooking with an improved cookstove. Lastly, we demonstrated that ABPM was a feasible and well-tolerated tool for BP assessment in a rural West African setting. For Project II in New York City, we first determined that there was a great deal of variability in indoor summer heat index (HI) between homes in association with similar outdoor conditions, and that this variability increased with increasing outdoor heat (Chapter 3). Our simulation of a moderate heat wave led us to conclude that the hottest 5% of the homes would reach peak indoor heat index (HI) values of 39°C. In a more extreme heat wave simulation, HI in the hottest 5% of homes reached a peak of 41oC and did not drop below 34oC for the entire nine- day simulated heat wave period. Our second indoor monitoring study yielded the following findings: in the summer season (Chapter 4), we found significant differences in indoor temperature and heat index according to the type of air conditioning (AC) in the home. Homes with central AC were the coolest, followed by homes with ductless AC, window AC, and no AC. Apartments on the top floor of a building were significantly hotter than other apartments regardless of the presence of AC. During the winter season (Chapter 5), median vapor pressure in our sample of apartments was 6.5mb. Comparing humidity levels in the apartments to a threshold of 10mb vapor pressure that has been proposed as protective against influenza virus transmission, levels of absolute humidity in the homes remained below this threshold for 86% of the winter: a total of over three months. Residential use of humidifiers was not associated with higher indoor humidity levels. Larger building size (above 100 units) was significantly associated with lower humidity, while the presence of a radiator heating system was non-significantly associated with higher humidity. Lastly, perceptions of indoor temperature and measured temperature were significantly associated in both the summer and the winter (Chapter 6), while sleep quality was inversely related to measured indoor temperature in the summer season only. Reports of heat- stress symptoms were associated with perceived, but not measured, temperature in the summer season. Conclusions: The work presented in this dissertation adds to a growing body of evidence on the importance of exposures in the domestic environment to health and well-being. The research reported here on household air pollution in Ghana documents an exposure-response relationship between air pollution from cookstoves and elevations in blood pressure, on both a chronic and an acute basis. As elevated BP is a known risk factor for cardiovascular disease (CVD), our research provides support for a plausible factor linking HAP exposure to CVD. Meanwhile, our research on temperature and humidity in New York City residences provides concrete data to supplement the very slim literature to date documenting these conditions in the home environment, where Americans spend over half their time. We conclude, first, that AC may not be fully protective against summertime heat risk, and second, that the levels of humidity we observed in residential environments are consistent with levels that have been shown to promote enhanced survival and transmission of respiratory viruses in experimental settings. We suggest that interventions that can reduce exposure to household air pollution and excess indoor heat can also mitigate climate change, and that with thoughtful planning we can improve health at the same time as we foster resiliency in the face of a changing climate.

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

Thesis (M.S.)--Uniformed Services University of the Health Sciences, 2005. / Typescript (photocopy).

This study explored preparatory students’ perceptions of the risk of contracting the Human Immuno-deficiency Virus (HIV) and sexually transmitted infections (STIs) in Ethopia. It utilised a non-experimental exploratory survey methodology. A range of findings was revealed. Most respondents (67.14%) were knowledgeable about HIV/AIDS and more than half of the respondents knew about STIs. A significant number of respondents (67.1%) were able to describe HIV transmission prevention methods. Twenty one percent of respondents were sexually active and 17.0% of these reported to have used condoms. Twenty nine percent and 4.25% of the respondents had selfperceived risk of contracting HIV infection and STIs respectively. In spite of increased awareness of HIV/AIDS, school youths still engage in high-risk sexual activities and believe that they are unlikely to contract the disease. The study findings have implications for practice, and recommendations are offered for further research / Health Studies / M.A. (Public Health)

Bien que la lutte contre le tabagisme passif se soit récemment accentuée, la fumée de tabac demeure un des principaux polluants atmosphériques d’intérieur. Le tabagisme passif génère des réactions cardiovasculaires néfastes qui, lors d’expositions répétées, augmentent le risque de mortalité cardiovasculaire. Le but des travaux réalisés a été de repenser la toxicité cardiovasculaire aiguë de la pollution de l’air par la fumée de tabac, en analysant plus particulièrement le rôle joué par la nicotine sur les déterminants endothéliaux et sympathiques du tonus vasculaire.<p>Nous avons tout d’abord caractérisé, chez des volontaires sains non-fumeurs, les réactions vasculaires provoquées par une heure d’inhalation passive de fumée de tabac ou de fumée non tabagique.1 Nos résultats démontrent que le tabagisme passif provoque une réflexion plus précoce de l’onde de pouls au niveau aortique ainsi qu’une perte de la capacité vasodilatatrice microvasculaire dépendante de l’endothélium. De plus, nous avons observé que ces réactions sont spécifiques à la fumée de tabac, et perdurent plusieurs dizaines de minutes après l’arrêt de l’exposition. Le stimulus nicotinique exerce un rôle prédominant dans les changements de réflexion d’onde de pouls. Cependant, l’interprétation du rôle joué par la nicotine dans la toxicité endothéliale du tabagisme passif est limitée in vivo par les effets de la nicotine sur d’autres déterminants du tonus vasculaire, tel que le système orthosympathique. <p>Nous avons dès lors spécifiquement comparé, à l’aide d’un modèle d’aorte isolée de rats, les effets d’extraits de fumée de tabac, de fumée non tabagique et de nicotine pure sur la fonction endothéliale et la production radicalaire.2 Chaque type de fumée a entraîné une augmentation similaire de la production radicalaire au sein des vaisseaux, mais seul l’extrait tabagique a altéré la relaxation vasculaire dépendante de l’endothélium. Dans les mêmes conditions, la nicotine pure a respecté l’intégrité fonctionnelle de l’endothélium, ce qui permet d’exclure son implication dans les effets délétères aigus du tabagisme passif sur l’endothélium vasculaire. <p>Nous avons ensuite déterminé, par des mesures directes du trafic nerveux autonome sur une population de volontaires sains non fumeurs, les effets directs de la nicotine sur le contrôle chémoréflexe périphérique du système orthosympathique.3 Nos résultats démontrent que des taux de nicotine similaires à ceux générés par une heure d’exposition au tabagisme passif augmentent la sensibilité d’une importante boucle réflexe participant à l’homéostasie du système nerveux autonome. <p>Enfin, malgré tous ces effets délétères de la nicotine observés chez le non-fumeur, nous avons établi que la perfusion myocardique du patient à risque coronaire élevé n’est toutefois pas altérée par une prise de nicotine sublinguale.4 <p>Les effets cardiovasculaires du tabagisme passif sont rapides, spécifiques, et réunissent des conditions de stimulation orthosympathique et de dysfonction endothéliale potentiellement néfastes pour la perfusion coronaire. Les effets sympathicomimétiques de la nicotine représentent l’axe prédominant de la toxicité cardiovasculaire aiguë du tabagisme passif. Toutefois, la nicotine pure n’altèrant pas la perfusion myocardique du patient à risque coronaire, son utilisation peut donc être encouragée dans l’aide au sevrage tabagique. <p> / Doctorat en Sciences médicales / info:eu-repo/semantics/nonPublished

No description available.

Indiana University-Purdue University Indianapolis (IUPUI) / Objectives: To examine the effect of a collaborative care program for late-life depression on risk of diabetes among depressed, older adults. Method: We conducted a 9-year follow-up study of 160 older, primary care patients with a depressive disorder but without diabetes enrolled at the Indiana sites of the Improving Mood-Promoting Access to Collaborative Treatment (IMPACT) trial. Results: Surprisingly, the rate of incident diabetes in the collaborative care group (22/80 = 27.5%) was twice the rate observed in the usual care group (11/80 = 13.7%). Cox proportional hazards models adjusted for randomization status (HR = 1.94, p = .076), demographic factors (HR = 1.94, p = .075), and additionally for diabetes risk factors (HR = 1.73, p = .157) indicated that the risk of incident diabetes did not differ between the collaborative care and usual care groups, with collaborative care patients remaining at a nonsignificant increased risk. Conclusions: Our novel findings suggest that depression may not be a casual risk factor for diabetes and that depression treatment may be insufficient to reduce the excess diabetes risk of depressed, older adults.

M. Tech. (Department of Biotechnology, Faculty of Applied and Computer Sciences), Vaal University of Technology. / Background: Increased serum homocysteine is well known as an independent cardiovascular risk factor. Hyperhomocysteinemia may be due to several factors such as nutritional deficiencies and genetics. The MTHFR C677T polymorphism is associated with increased serum homocysteine. Folate and vitamin B12 play essential roles in lowering homocysteine levels. Limitations have been identified using serum vitamin B12 as a marker for vitamin B12 status due to lack an efficient of test. Holotranscobalamin has been reported as a more accurate marker for vitamin B12 status. Cardiovascular risk due to hyperhomocysteinemia has been confirmed among the elderly in Sharpeville. Knowledge of the prevalence of MTHFR C677T polymorphism among Black elderlies in South Africa is limited. Objectives: The main aim of the study was to evaluate the prevalence of MTHFR C677T polymorphism as a cardiovascular risk in an elderly black population in Sharpeville. Correlations between the presence of MTHFR C677T polymorphism and homocysteine metabolic markers were evaluated. Holotranscobalamin as a diagnostic test for vitamin B12 status was also assessed in this study. Materials and methods: This study was ethically approved by the Vaal University of Technology ethics committee (20140827-1ms). It was an observational, experimental study conducted in 102 elderly (≥60 years) attending the day-care centre in Sharpeville. Real-Time PCR was used to determine MTHFR genotypes. Folate and vitamin B12 were measured with AIA-PACK. Homocysteine levels were determined with an automated Konelab™ 20i and holotranscobalamin by ELISA. STATA 12 software was used for analysis of descriptive and inferential statistics. Results: The prevalence of MTHFR C677T polymorphism in this sample population was 19%. Heterozygous CT single nucleotide polymorphism was 17% and mutant homozygous TT was 2%. The majority (81%) of the subjects had wild type homozygous CC genotypes. No associations were found between MTHFR C677T genotypes and homocysteine and folate levels. Hyperhomocysteinemia was high (54%) and low (5%) folate deficiency found. No vitamin B12 deficiency was found however 7% were on the category of likely to be deficient. Sensitivity and specificity of holotranscobalamin were 100% and 95% respectively. Conclusion: The conclusions drawn from the study is that the prevalence of MTHFR C677T polymorphism is low within elderly in Sharpeville. There is a high risk of cardiovascular disease as a result of high prevalence of hyperhomocysteinemia. An intervention to lower homocysteine concentration of elderlies residing in Sharpeville is needed. Other genetic predisposing factors of increased homocysteine levels should be investigated.

Background: Herpes Simplex Virus Type 2 (HSV 2) is one of the most common sexually transmitted infections (STIs) worldwide. HSV 2 infection is a risk factor for the acquisition and transmission of other STIs. Aim: The aim of this study is to determine prevalence and predictors of HSV 2 infection in Durban, South Africa by using available data that has not been previously analysed for the purpose of adding scientific evidence to the existing body of knowledge relating to HSV 2. Method: The study involves secondary analyses of data collected as a prospective study which enrolled women who participated in a clinical trial. A total of 3472 sexually active women were screened in the primary study from two clinics in Durban. All consenting participants were tested for HIV, HSV 2, Trichomonas vaginalis (TV), Neisseria gonorrhoea (NG) and Chlamydia trachomatis (CT) infection. Results: There were 2532 women who had HSV 2 giving a prevalence of 73%. Of these, 53% also tested positive for HIV infection. In univariate analysis, co-infection with HIV was strongly associated with HSV2 (Odds Ratio (OR): 7.4, 95% Confidence Interval (CI): 6.0, 9.1, p<0.001). There was also an association between other STIs, such as CT, NG and syphilis and HSV 2, although only NG was significantly associated with prevalent of HSV 2 (OR: 2.3, 95% CI: 1.3, 4.1, p=0.005). Women older than 25 years of age more likely to have HSV 2 (OR: 2.4, 95% CI: 2.0,2.8, p<0.001). A risk of being infected with HSV 2 increased with the number of reported lifetime sexual partners Those with two and three or more were 2,5 and 4.6 times more likely to have HSV2 respectively (OR: 2.5, 95% CI: 2.1,3.1, p<0.001 and OR: 4.6, 95% CI: 3.8, 5.6, p<0.001 respectively). Women who had less than high school education were also found to have higher risk for HSV 2. Conclusion: The secondary analysis showed a high prevalence of HSV 2 infection and a strong association of HSV 2 and HIV. A significant association of HSV 2 was noted in women having more than two sex partners and lower high school education. Therefore, it is recommended that screening for HSV 2 among high risk populations be incorporated into the STI screening and treatment packages. / Prevalence and risk factors associated with HSV 2 / Herpes Simplex Virus Type 2 / HSV 2 / Department of Health Studies / M. (Public health)

Background: Herpes Simplex Virus Type 2 (HSV 2) is one of the most common sexually transmitted infections (STIs) worldwide. HSV 2 infection is a risk factor for the acquisition and transmission of other STIs. Aim: The aim of this study is to determine prevalence and predictors of HSV 2 infection in Durban, South Africa by using available data that has not been previously analysed for the purpose of adding scientific evidence to the existing body of knowledge relating to HSV 2. Method: The study involves secondary analyses of data collected as a prospective study which enrolled women who participated in a clinical trial. A total of 3472 sexually active women were screened in the primary study from two clinics in Durban. All consenting participants were tested for HIV, HSV 2, Trichomonas vaginalis (TV), Neisseria gonorrhoea (NG) and Chlamydia trachomatis (CT) infection. Results: There were 2532 women who had HSV 2 giving a prevalence of 73%. Of these, 53% also tested positive for HIV infection. In univariate analysis, co-infection with HIV was strongly associated with HSV2 (Odds Ratio (OR): 7.4, 95% Confidence Interval (CI): 6.0, 9.1, p<0.001). There was also an association between other STIs, such as CT, NG and syphilis and HSV 2, although only NG was significantly associated with prevalent of HSV 2 (OR: 2.3, 95% CI: 1.3, 4.1, p=0.005). Women older than 25 years of age more likely to have HSV 2 (OR: 2.4, 95% CI: 2.0,2.8, p<0.001). A risk of being infected with HSV 2 increased with the number of reported lifetime sexual partners Those with two and three or more were 2,5 and 4.6 times more likely to have HSV2 respectively (OR: 2.5, 95% CI: 2.1,3.1, p<0.001 and OR: 4.6, 95% CI: 3.8, 5.6, p<0.001 respectively). Women who had less than high school education were also found to have higher risk for HSV 2. Conclusion: The secondary analysis showed a high prevalence of HSV 2 infection and a strong association of HSV 2 and HIV. A significant association of HSV 2 was noted in women having more than two sex partners and lower high school education. Therefore, it is recommended that screening for HSV 2 among high risk populations be incorporated into the STI screening and treatment packages. / Prevalence and risk factors associated with HSV 2 / Herpes Simplex Virus Type 2 / HSV 2 / Department of Health Studies / M. (Public health)