published_or_final_version / abstract / Medicine / Doctoral / Doctor of Philosophy

Made available in DSpace on 2016-08-10T10:55:13Z (GMT). No. of bitstreams: 1 Amanda Eliza Goulart de Souza Britto.pdf: 709817 bytes, checksum: 09dadfee23fc97a74a25c1bb5e0136bb (MD5) Previous issue date: 2007-03-27 / A preliminary study was carried out in the region around Brasília, in the area under the influence of the Corumbá IV Hydroelectric Power Plant where, through the recovered epidemiological data from the Reports Notification System (SINAN). These data were used for a preliminary evaluation of the impact of the construction of a hydroelectric power plant on diseases, before, during, and after the insertion of this kind of enterprise, divided in bacterioses, protozoonoses, and viruses. The data were compared with the data of occurrence of diseases in the region under the direct influence of this power plant and evaluated in relation of the environmental impact on the population health of other cities around Brasília, in this study interpreted as included in the indirect influence area. Despite being a preliminary study the results suggest preoccupation for some infirmities and could be suggestive for future studies in an area of extreme importance in public health. / Um estudo preliminar foi realizado na região do entorno de Brasília, na área de influência da Usina Hidrelétrica (UHE) Corumbá IV, através do resgate de dados epidemiológicos do Sistema de Notificação de Agravos (SINAN). Esses dados foram utilizados para uma avaliação preliminar do impacto da construção de uma usina hidrelétrica em doenças, antes, durante e após a inserção desse tipo de empreendimento, divididos em bacterioses, protozoonoses e viroses. Os dados foram comparados com os dados de ocorrência das doenças na região de influência direta dessa UHE e avaliados em relação ao impacto ambiental sobre a saúde da população de outras cidades do entorno de Brasília, nesse trabalho interpretadas como dentro da área de influência indireta. Apesar de ser um estudo preliminar, os resultados sugerem preocupações para algumas enfermidades e pode ser sugestivo para estudos futuros mais aprofundados em uma área de extrema importância em saúde pública.

Frente à recente detecção em território brasileiro de Monilina laxa, que assim como M. fructicola, é causadora da podridão parda do pessegueiro, e à falta de informações sobre a epidemiologia dos patógenos causadores da doença em regiões subtropicais, surgiu a necessidade deste trabalho, que teve por objetivos determinar as melhores condições de temperatura e molhamento para o desenvolvimento de M. fructicola e M. laxa in vitro e para a infecção e colonização pêssegos por conídios dos patógenos. Quatro isolados de M. fructicola e um isolado de M. laxa, provenientes de plantios do Estado de São Paulo e mantidos no laboratório de Epidemiologia da ESALQ, foram estudados. Foram avaliados os efeitos da temperatura e da duração do molhamento na germinação dos conídios in vitro e o efeito da temperatura no crescimento micelial e na esporulação dos patógenos. Ensaios para determinar a sensibilidade dos patógenos ao fungicida iminoctadina também foram conduzidos. Adicionalmente, pêssegos maduros foram adquiridos, feridos, inoculados com suspensão de conídios e incubados em diferentes temperaturas sob diferentes períodos de câmara úmida. Diariamente incidência e severidade foram avaliadas. A esporulação foi avaliada ao final de cada tratamento. A faixa ótima de temperatura para germinação de conídios de M. laxa, de 5 a 30ºC, é maior que a de M. fructicola, de 10 a 30ºC. O período de molhamento não teve influência na germinação dos conídios. A melhor faixa de temperatura para crescimento micelial tanto de M. fructicola quanto M. laxa de foi de 20 a 25ºC. A esporulação de M. laxa foi inversamente proporcional à temperatura de incubação. Não houve relação entre temperatura e produção de esporos em M. fructicola. Ambas as espécies mostraram-se sensíveis, in vitro, à molécula iminoctadina. A incidência da podridão parda foi superior a 80,9% em todos os tratamentos, para as duas espécies fúngicas. A 10ºC os períodos de incubação e de latência foram menores para M. laxa que para M. fructicola. A faixa ótima de temperatura para o desenvolvimento de lesões variou de 15 a 25ºC para os dois patógenos. A esporulação dos patógenos não mostrou relação com a temperatura nos ensaios in vivo. Diferenças nos sinais da espécie do patógeno foram observados nas lesões. / Due to the recent detection in Brazil of Monilinia laxa, that similar to M. fructicola causes the brown rot of peaches, and the lack of information about the epidemiology of the causal agents of this disease from subtropical regions, raised the need of such a study, which the aims were to determine the best temperature and wetness duration conditions to the development of M. fructicola and M. laxa in vitro and to infection and colonization of peaches by conidia from both pathogens. Four M. fructicola isolates and one M. laxa isolate, collected from infected fruit of São Paulo orchards and maintained at the Epidemiology Laboratory at ESALQ, were studied. Temperature and wetness duration effects on conidia germination in vitro and temperature effects on mycelial growth and sporulation of pathogens were evaluated. Trials to evaluate the sensitivity of isolates to the fungicide iminoctadine were also conducted. Furthermore, mature peaches were wounded on the surface, inoculated with a conidia suspension and incubated at different temperatures during different wet chamber periods. Incidence and severity of the disease were evaluated daily. Sporulation was evaluated at the end of each treatment. The favorable range of temperature to conidia germination of M. laxa, from 5 to 30ºC, was greater than M. fructicola range, from 10 to 30ºC. The wetness duration showed no influence on conidia germination. The best range of temperature for mycelial growth of both M. fructicola and M. laxa was from 20 to 25ºC. Sporulation of M. laxa showed an inverse relationship to the incubation temperature. No relationship between temperature and conidia production was found for M. fructicola. Both species were sensitive to the iminoctadine fungicide in vitro. Incidence of brown rot was greater than 80.9% in all treatments, for both species. At 10ºC incubation and latency periods were shorter for M. laxa than for M. fructicola. The best temperatures for lesion development varied between 15 and 25ºC for both pathogens. Sporulation of the two species showed no relationship to the temperature on the in vivo trials. Visual differences were observed on pathogen symptoms on fruit.

The broad aim of this dissertation is to understand the early impact of HPV vaccination in females at the population level. Three important public health questions are addressed: 1) Is HPV vaccination doing what is expected: decreasing the prevalence of vaccine-type HPV 6, 11, 16 and 18 which are etiologically linked to invasive cervical cancer and genital warts?; 2) Is there evidence of beneficial cross-protection (decreased prevalence) of any of the other non-vaccine-targeted high-risk (HR) HPV genotypes?; and 3) With the expected decline of HPV 16 and 18, are there deleterious virological consequences, such as type-replacement (increased prevalence) with a rise of non-vaccine-targeted HR HPV? In the first chapter, I assess and synthesize peer-reviewed literature published from 2007 to 2013 that documented early impact of HPV vaccination. Seventeen ecological studies were stratified into three tiers based on degree of vaccination impact (cervical abnormalities, genital warts, and HPV DNA) and incidence or prevalence in samples from a pre-HPV vaccination time period (pre-2007) with that of a post-vaccination time period (post-2007) were compared. In the second chapter, I investigate vaccine-type HPV prevalence changes between pre- and post-vaccine periods in over 8,000 females aged 14-59 years enrolled in the NHANES HPV Vaginal Swab Surveys from 2003-2010. In the third chapter, I test for evidence of non-vaccine-targeted HR HPV genotypic cross-protection and type-replacement in NHANES Survey females from the pre- and post-vaccine periods. Finally, I conclude the dissertation with a summary of the findings and a discussion of the public health impltcations and offer suggestions for future research.

Tang, Suk Yan Amy. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (leaves [207]-[227]). / Abstracts in English and Chinese. / ACKNOWLEDGEMENTS / ABSTRACTS / TABLE OF CONTENTS / "LIST OF APPENDIX, TABLES & FIGURES" / Chapter CHAPTER ONE --- INTRODUCTION --- p.1 / Chapter 1.1 --- Cerebrovascular disease --- p.1 / Chapter 1.1.1 --- Ischemic Stroke --- p.1 / Chapter 1.1.2 --- Hemorrhagic Stroke --- p.2 / Chapter 1.2 --- Laboratory diagnosis --- p.3 / Chapter 1.2.1 --- Transcranial Doppler ultrasonography --- p.4 / Chapter 1.2.1.1 --- Normal Brain --- p.4 / Chapter 1.2.1.2 --- Intracranial Large Artery Stenosis --- p.5 / Chapter 1.3 --- Asymptomatic Intracranial Stenosis --- p.6 / Chapter CHAPTER TWO --- LITERATURE REVIEW --- p.7 / Chapter 2.1 --- Global Stroke Facts --- p.7 / Chapter 2.2 --- Stroke Studies --- p.7 / Chapter 2.2.1 --- Risk profile of stroke --- p.7 / Chapter 2.2.2 --- Stroke epidemiological study --- p.8 / Chapter 2.2.2.1 --- Incidence --- p.8 / Chapter 2.2.2.2 --- Mortality --- p.10 / Chapter 2.2.2.3 --- Increased stroke rates with increased age --- p.12 / Chapter 2.2.2.4 --- Associated disease in stroke subjects --- p.12 / Chapter 2.2.3 --- Stroke risk factors --- p.13 / Chapter 2.3 --- Stroke Impact --- p.14 / Chapter 2.3.1 --- Stroke patients --- p.14 / Chapter 2.3.2 --- Medical burden --- p.15 / Chapter 2.3.3 --- Socioeconomic burden --- p.16 / Chapter 2.4 --- Stroke Prevention --- p.17 / Chapter 2.5 --- Stroke Facts in Hong Kong --- p.19 / Chapter 2.6 --- Stroke Facts in China --- p.21 / Chapter 2.7 --- Asymptomatic Intracranial Stenosis in Asian Subjects --- p.22 / Chapter 2.7.1 --- Asymptomatic individuals --- p.22 / Chapter 2.7.2 --- Intracranial occlusive disease --- p.23 / Chapter 2.8 --- Transcranial Doppler Sonography --- p.25 / Chapter CHAPTER THREE --- AIM & OBJECTIVES OF THE RESEARCH --- p.30 / Chapter 3.1 --- Aim of the research --- p.30 / Chapter 3.2 --- Objectives of this research --- p.30 / Chapter CHAPTER FOUR --- "CLINIC-BASED CROSS-SECTIONAL SCREENING IN AN URBAN CITY 226}0ؤ HONG KONG, THE PEOPLE'S REPUBLIC OF CHINA" --- p.31 / Chapter 4.1 --- Background & Purpose --- p.31 / Chapter 4.2 --- Methods --- p.34 / Chapter 4.2.1 --- Defining the population --- p.34 / Chapter 4.2.2 --- Procedures --- p.36 / Chapter 4.2.2.1 --- Standardized TCD Report Form --- p.39 / Chapter 4.2.2.2 --- Transcranial Doppler Screening --- p.39 / Chapter 4.2.2.3 --- Data collected --- p.40 / Chapter 4.2.3 --- Defining the Risk Factors --- p.43 / Chapter 4.3 --- Statistical Analyses --- p.45 / Chapter 4.3.1 --- Research Design --- p.46 / Chapter 4.3.2 --- Descriptive Summary --- p.46 / Chapter 4.3.2.1 --- Cross-tabulated between Gender --- p.46 / Chapter 4.3.2.2 --- Cross-tabulated between Normal & Abnormal MCA status --- p.47 / Chapter 4.3.3 --- Measures for Association --- p.48 / Chapter 4.3.3.1 --- Univariate analysis --- p.48 / Chapter 4.3.3.2 --- Multivariate analysis --- p.48 / Chapter 4.3.4 --- Modeling the Risks --- p.50 / Chapter 4.3.5 --- nfluence of the number of associated risk factors on the MCA status --- p.50 / Chapter 4.4 --- Result --- p.51 / Chapter 4.4.1 --- Baseline characteristics of all screened subjects by Gender --- p.51 / Chapter 4.4.1.1 --- Age by Gender --- p.53 / Chapter 4.4.1.2 --- "Medical History of HT, DM, Hyperlipidemia, IHD, Retinopathy and Albuminuria by Gender" --- p.55 / Chapter 4.4.1.3 --- Social habit in Smoking by Gender --- p.56 / Chapter 4.4.1.4 --- Body Mass Index and Waist-to-Hip Ratio by Gender --- p.57 / Chapter 4.4.2 --- Diseased Middle Cerebral Artery --- p.61 / Chapter 4.4.3 --- Characteristics between subjects with Normal TCD result and Abnormal TCD result in the MCA status --- p.62 / Chapter 4.4.3.1 --- Age --- p.64 / Chapter 4.4.3.2 --- Gender --- p.67 / Chapter 4.4.3.3 --- "Medical History of HT, DM, Hyperlipidemia, IHD, Retinopathy and Albuminuria" --- p.67 / Chapter 4.4.3.4 --- Social habit in cigarette smoking --- p.68 / Chapter 4.4.3.5 --- Body Mass Index and Waist-to-Hip Ratio --- p.71 / Chapter 4.4.3.6 --- "Other Measurements - on Blood Pressure, Fasting Plasma Glucose, HbAlc, Lipid profiles and Fibrinogen" --- p.79 / Chapter 4.4.4 --- Unadjusted Odds Ratio --- p.84 / Chapter 4.4.4.1 --- By contingency table method --- p.84 / Chapter 4.4.4.2 --- By logistic regression model --- p.86 / Chapter 4.4.5 --- Adjusted Odds Ratio --- p.92 / Chapter 4.4.5.1 --- Entering all explanatory variables: --- p.92 / Chapter 4.4.5.2 --- Using Forward and Backward Stepwise methods with the probability for entry of 0.05 and probability for removal of 0.10: --- p.95 / Chapter 4.4.5.3 --- Applying the Model-Building Strategy: --- p.100 / Chapter 4.4.6 --- Comparing the final fitted multiple logistic regression models made by the three approaches ： --- p.103 / Chapter 4.4.7 --- Probability and Odds derived from the logistic regression model --- p.110 / Chapter 4.4.8 --- Relationship between the diseased MCA and the number of significant risk indicators that the subjects associated with..… --- p.112 / Chapter 4.4.8.1 --- Logistic regression analysis on number of risk indicators associated with the MCA status --- p.115 / Chapter 4.5 --- Discussion --- p.118 / Chapter 4.5.1 --- Research Design --- p.118 / Chapter 4.5.1.1 --- Advantage --- p.118 / Chapter 4.5.1.2 --- Disadvantage --- p.118 / Chapter 4.5.2 --- Sampling --- p.119 / Chapter 4.5.3 --- Data collected and Outcome variable classified --- p.119 / Chapter 4.5.3.1 --- Medical Record - Patients Characteristics --- p.119 / Chapter 4.5.3.2 --- Transcranial Doppler - Middle Cerebral Artery status --- p.120 / Chapter 4.5.4 --- Statistical Analyses --- p.121 / Chapter 4.5.4.1 --- Odds Ratio --- p.121 / Chapter 4.5.4.2 --- Logistic Regression Model --- p.122 / Chapter 4.5.4.3 --- Sources of Error --- p.123 / Chapter 4.5.5 --- Result --- p.125 / Chapter 4.5.5.1 --- Prevalence --- p.125 / Chapter 4.5.5.2 --- Risk indicators --- p.126 / Chapter CHAPTER FIVE --- "POPULATION-BASED CROSS-SECTIONAL SURVEY IN A RURAL VILLAGE OF HENAN, PEOPLE'S REPUBLIC OF CHINA" --- p.134 / Chapter 5.1 --- Background & Purpose --- p.134 / Chapter 5.2 --- Methods --- p.135 / Chapter 5.2.1 --- Defining the Population --- p.135 / Chapter 5.2.2 --- Procedures --- p.135 / Chapter 5.2.2.1 --- Standardized Screening Form --- p.136 / Chapter 5.2.2.2 --- Transcranial Doppler Examination --- p.137 / Chapter 5.2.3 --- Defining the Risk Factors --- p.137 / Chapter 5.3 --- Statistical Analyses --- p.140 / Chapter 5.3.1 --- Research Design --- p.141 / Chapter 5.3.2 --- Descriptive Summary --- p.141 / Chapter 5.3.2.1 --- Cross-tabulated between Gender --- p.141 / Chapter 5.3.2.2 --- Cross-tabulated between With & Without intracranial large artery stenosis --- p.142 / Chapter 5.3.3 --- Measures for Association --- p.143 / Chapter 5.3.3.1 --- Univariate analysis --- p.143 / Chapter 5.3.3.2 --- Multivariate analysis --- p.143 / Chapter 5.3.4 --- Modeling the Risks --- p.144 / Chapter 5.3.5 --- Influence of the number of associated risk factors on the prevalence of intracranial large artery stenosis --- p.144 / Chapter 5.4 --- Result --- p.145 / Chapter 5.4.1 --- Baseline characteristics of all examined villagers by Gender --- p.145 / Chapter 5.4.1.1 --- Age by Gender --- p.147 / Chapter 5.4.1.2 --- "Medical History of HT, DM and Heart disease by Gender" --- p.149 / Chapter 5.4.1.3 --- Social habit in Cigarette smoking and Alcoholic drinking by Gender --- p.149 / Chapter 5.4.1.4 --- "Family History of HT, DM, Stroke and Heart disease by Gender" --- p.149 / Chapter 5.4.1.5 --- Body Mass Index and Waist-to-Hip Ratio by Gender --- p.150 / Chapter 5.4.2 --- Distribution of the Diseased intracranial artery --- p.154 / Chapter 5.4.3 --- Characteristics between subjects with and without intracranial large artery stenosis --- p.155 / Chapter 5.4.3.1 --- Age --- p.157 / Chapter 5.4.3.2 --- Gender --- p.158 / Chapter 5.4.3.3 --- "Medical History of HT, DM and Heart disease" --- p.158 / Chapter 5.4.3.4 --- Social habit in cigarette smoking and alcohol drinking --- p.158 / Chapter 5.4.3.5 --- "Family History of HT, DM, Stroke and Heart Disease" --- p.159 / Chapter 5.4.3.6 --- Body Mass Index and Waist-to-Hip Ratio --- p.160 / Chapter 5.4.3.7 --- Other Measurements - on BP and Urine Glucose --- p.163 / Chapter 5.4.4 --- Unadjusted Odds Ratio --- p.165 / Chapter 5.4.4.1 --- By contingency table method --- p.165 / Chapter 5.4.4.2 --- By logistic regression model --- p.166 / Chapter 5.4.5 --- Adjusted Odds Ratio --- p.172 / Chapter 5.4.5.1 --- Entering all explanatory variables: --- p.172 / Chapter 5.4.5.2 --- Using the Stepwise methods available with the probability for entry is 0.05 and 0.10 for removal: --- p.175 / Chapter 5.4.5.3 --- Applying the Model-Building Strategy: --- p.180 / Chapter 5.4.6 --- Comparing the final multiple logistic regression models by the three approaches： --- p.182 / Chapter 5.4.7 --- Probability and Odds derived from the logistic regression model --- p.189 / Chapter 5.4.8 --- Relationship between the transcranial Doppler result on Intracranial large artery and the number of significant risk indicators that the subjects associated with --- p.190 / Chapter 5.4.8.1 --- Logistic Regression Model --- p.192 / Chapter 5.5 --- Discussion --- p.196 / Chapter 5.5.1 --- Research Design --- p.196 / Chapter 5.5.1.1 --- Advantage --- p.196 / Chapter 5.5.1.2 --- Disadvantage --- p.196 / Chapter 5.5.2 --- Sampling --- p.197 / Chapter 5.5.3 --- Data collected and the Outcome variable classified --- p.197 / Chapter 5.5.3.1 --- Self-Reported - Subjects Characteristics --- p.197 / Chapter 5.5.3.2 --- Transcranial Doppler - Intracranial Large Artery status --- p.198 / Chapter 5.5.4 --- Statistical Methods --- p.199 / Chapter 5.5.4.1 --- Odds Ratio --- p.199 / Chapter 5.5.4.2 --- Logistic Regression --- p.199 / Chapter 5.5.4.3 --- Sources of Error --- p.199 / Chapter 5.5.5 --- Result --- p.200 / Chapter 5.5.5.1 --- Prevalence --- p.200 / Chapter 5.5.5.2 --- Risk Indicators --- p.201 / Chapter CHAPTER SIX --- CONCLUSION --- p.204 / Chapter 6.1 --- The Clinic-based study of diseased middle cerebral artery among asymptomatic hong kong chinese --- p.204 / Chapter 6.2 --- The Population-base study of intracranial large artery stenosis among mid-aged & above chinese in rural china --- p.205 / REFERENCES / APPENDIX / Appendix I Neuroimaging - Transcranial Doppler Ultrasonography / Appendix II Statistical Methods / "Appendix III (a) Standardized TCD report form used in PWH, Hong Kong (b) Standardized Screening Form used In Yuzhou, China" / Appendix IV The ICD 9th Revision - Disease of the Circulatory System / "Appendix V Prospective Hospital-Based study in Asia, AASAP (a) Standardized Data Collection From used in AASAP" / Appendix VI Contributed in published papers

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For explanation and prediction of the evolution of infectious diseases in populations, researchers often use simplified mathematical models for simulation. We believe that the results from these models are often questionable when the epidemic dynamics becomes more complex, and that developing more realistic models is intractable. In this dissertation we propose to simulate infectious disease propagation using dynamic and complex networks. We present the Simulator of Epidemic Evolution using Complex Networks (SEECN), an expressive and high-performance framework that combines algorithms for graph generation and various operators for modeling temporal dynamics. For graph generation we use the Kronecker algorithm, derive its underlying statistical structure and exploit it for a variety of purposes. Then the epidemic is evolved over the network by simulating the dynamics of the population and the epidemic simultaneously, where each type of dynamics is performed by a separate operator. All dynamics operators can be fully and independently parameterized, facilitating incremental model development and enabling different influences to be toggled for differential analysis. As a prototype, we simulate two relatively complex models for the HIV epidemic and find a remarkable fit to reported data for AIDS incidence and prevalence. Our most important conclusion is that the mere dynamics of the HIV epidemic is sufficient to produce rather complex trends in the incidence and prevalence statistics, e.g. without the introduction of particularly effective treatments at specific times. We show that this invalidates assumptions and conclusions made previously in the literature, and argue that simulations used for explanation and prediction of trends should incorporate more realistic models for both the population and the epidemic than is currently done. In addition, we substantiate a previously predicted paradox that the availability of Highly Active Anti-Retroviral Treatment likely causes an increased HIV incidence.

Diss. (sammanfattning) Uppsala : Sveriges lantbruksuniv., 2007. / Härtill 5 uppsatser.

Thesis (M. Sc.) Uppsala : Sveriges lantbruksuniv.

Diss. (sammanfattning) Uppsala : Sveriges lantbruksuniversitet. / Härtill 5 uppsatser.