published_or_final_version / Biological Sciences / Doctoral / Doctor of Philosophy

The purpose of this study was to determine the prevalence of known etiological factors in mildly mentally handicapped students across minority and nonminority groups and to examine the similarities of these patterns. A comparison of early diagnoses was also made. The total population of all children labeled Educable Mentally Handicapped (EMH) and attending regular elementary schools within one of the largest districts in the southwest served as the sample for the present study. There were 128 children, 64 minorities and 64 nonminorities. The student records were reviewed for data regarding etiological factors, previous diagnoses and early medical factors. A pilot study which involved administering a questionnaire to a sample to twenty-eight social workers was conducted to ascertain the validity of obtained data. Eight specific hypotheses were addressed. A Chi-Square analysis yielded information about the patterns of category similarities (congenital, prenatal, perinatal, postnatal and familial), between two groups as well as the presence of professional diagnosis. A set of five factorial analysis of variance were performed to examine the impact of age, number of symptoms, presence of professional diagnosis and length of hospital stay on IQ scores of children in both groups. A discriminant function analysis was performed to determine the discriminatory power of four variables (IQ, length of hospital stay, number of symptoms and presence of professional diagnosis). The prevalence of perinatal and postnatal symptoms and diagnoses occurred with high frequency for both groups. Congenital factors occurred significantly more for the nonminority group. The findings indicated that there were no significant differences across minority and nonminority groups in terms of intellectual functioning due to the impact of the four previously mentioned variables. Consistent with the ANOVA results, the information obtained from the discriminant function analysis suggests similarity of the two groups in terms of the four variables. The results were discussed in relation to the utility of early etiological information and the importance of such research. The implications of such findings for placement of children in general in these classes or for the children from minority groups in particular, were emphasized.

The causes of childhood cancers are not well understood. That infections are believed to play an important role in childhood cancer development is of particular interest in sub-Saharan Africa, where infectious diseases are common. The objectives of this thesis were to identify childhood cancers associated with HIV, malaria, EBV and HHV-8, and to investigate child and maternal factors associated with Burkitt lymphoma and Kaposi sarcoma. In Blantyre, Malawi, 305 children diagnosed with cancer and 212 of their mothers, were recruited. Risk factor data were collected using a brief questionnaire and blood samples tested for infections. Case-control analyses were conducted to compare 148 Burkitt lymphoma cases and 22 Kaposi sarcoma case with a control group comprising 104 children with cancers other than those known to be associated with HIV. The prevalence of HIV was 6% among children with Burkitt lymphoma and 2% in controls (OR=12.4, 95% CI 1.3 to 116.2). Tumour risk increased with increasing litres of antibodies against EBV and malaria. In comparison with those who had low titres against both EBV and malaria, the highest risk of Burkitt lymphoma was among those with high titres against both infections (OR=13.2, 95% CI 3.8 to 46.6). Reported use of mosquito nets was protective against Burkitt lymphoma. The prevalence of HIV was 81% among children with Kaposi sarcoma (OR=762.7, 95% CI 44 to 13376), and risk increased with increasing HHV-8 antibodies. Prevalence of infections was also examined among children with other cancer types and no associations were identified, although the number of cases was small. Few maternal factors were found to be associated with cancer in children. This research demonstrates that infections play a particularly important role in increasing the risk of Burkitt lymphoma and Kaposi sarcoma in children in sub- Saharan Africa. Prevention or early treatment of these infections may be vital in the control of childhood cancer.

A research report submitted to the Faculty of Health Sciences, School of Public Health, University of the Witwatersrand, Johannesburg, in partial fulfillment of the requirements for the degree of Master of Public Health: Occupational Hygiene, Johannesburg, 2012 / The aim of the study was to determine if the gold mine under study achieved the 2008 elimination of silicosis occupational hygiene milestones as set out by the South African mining industry in 2003. To identify high risk quartz exposed occupations within the conventional stope and TM³ stope employees of an underground gold mine between July 2008 and June 2010; to describe the personal quartz exposure of conventional stope and TM³ stope employees in an underground gold mine between July 2008 and June 2010; and to compare the time weighted average (TWA) quartz exposures between the conventional stope and TM³ stope to the Department of Mineral Resources-Occupational Exposure Limit (DMR-OEL) of 0.1 mg/m3, the National Institute of Occupational Safety and Health-Recommended Exposure Limit (NIOSH-REL) of 0.05 mg/m3 and the American Conference of Government Industrial Hygienists-Threshold Limit Value (ACGIHTLV) of 0.025 mg/m3.

ZAMPRONIO, C. D. P. A deficiência auditiva nas cidades abrangidas pela DRS-6: caracterização da população atendida na Divisão de Saúde Auditiva do HRAC- USP Bauru. 2009. 86 f. Dissertação (Mestrado em Saúde na Comunidade). Faculdade de Medicina de Ribeirão Preto-USP. A deficiência auditiva presente ao nascimento ou estabelecida na mais tenra idade interfere significativamente no processo de desenvolvimento da criança. Quando ocorre em uma pessoa adulta pode levar a um quadro de isolamento, podendo torná-la dissociada da sua comunidade, limitando sua capacidade de atuar com independência e autonomia perante a sociedade. Assim, qualquer distúrbio no processo de audição normal, seja qual for sua causa, tipo ou severidade, constitui uma alteração auditiva que pode e deve ser evitada, em benefício da saúde do indivíduo e da sociedade como um todo. Objetivo: Caracterização da deficiência auditiva nos pacientes atendidos na Divisão de Saúde Auditiva (DSA), do Hospital de Reabilitação de Anomalias Craniofaciais (HRAC), Universidade de São Paulo (USP), residentes nas 68 cidades do estado de São Paulo abrangidas pelo Departamento Regional de Saúde (DRS)-6, segundo algumas variáveis como: faixa etária, gênero, nível socioeconômico, escolaridade, etiologia, grau e tipo da deficiência auditiva. Métodos: Levantamento dos pacientes que iniciaram tratamento na DSA do HRAC/USP, no período 1998 a 2007, residentes nas cidades abrangidas pelo DRS-6 e que tiveram diagnóstico audiológico concluído em deficiência auditiva em pelo menos uma orelha. Para melhor visualização das características da amostra estudada, os 692 sujeitos foram separados em dois grupos, sendo um grupo da cidade de Bauru e outro das demais cidades da DRS-6. Resultados: Não houve predomínio entre os gêneros; a população idosa representou um número significativo de sujeitos quando comparada às demais faixas etárias; a maioria dos sujeitos pertence à classe socioeconômica baixa. Constatou-se que as principais etiologias encontradas em ambos os grupos foram: otite, otosclerose e presbiacusia. Conclusão: Conhecendo as características de uma população, outras pesquisas poderão ser feitas e mudanças realizadas para melhoria na qualidade do atendimento ao deficiente auditivo, principalmente quanto à precisão do diagnóstico diferencial. / ZAMPRONIO, C. D. P. Hearing deficiency in DRS - 6 cities: characterization of people attended at Hearing Health Division of HRAC-USP Bauru. 2009. 86 f. Dissertation (Master Degree). Faculdade de Medicina de Ribeirão Preto-USP. Hearing loss, present at birth time or established at an early age, presents a significant influence upon child development process. When it occurs in an adult individual it may lead to some isolation, separating him or her from its community, limiting his ability to act independently and autonomously toward society. Thus, any disturbance in normal hearing process, whatever the cause, severity or type might be, means a hearing change that may and can be avoided for the benefit of the health of the individual and the whole society. Objective: Characterization of hearing loss in patients attended at Hearing Health Division (HHD) of the Hospital for Craniofacial Anomalies Rehabilitation (HRAC), living in the 68 cities of the State of Sao Paulo comprising the Regional Health Department (DRS-6), according to some variables like age range, gender, socioeconomic level, school range, etiology, grade and kind of hearing loss. Methods: Survey of patients that started a treatment at the HHD of HRAC/USP, during the period from 1998 to 2007, living in the cities comprising the DRS-6 and that received an audiologic diagnosis of hearing loss at least in one of the ears. For a better visualization of the studied sample, the 692 subjects were divided in two groups, one living in Bauru and one living in the other cities of DRS-6. Results: There has not been any predominance between genders; elderly population represented a significant number of subjects compared to the other age ranges and most subjects belonged to low socioeconomic class. It was observed that the main etiologies found for both groups were: otitis, otosclerosis, and presbyacusis. Conclusion: Knowing the characteristics of a population, other surveys may be performed and changes made to make better the attendance quality for hearing loss people and, especially, the accuracy of differential diagnosis.

by Wai-keung Leung. / Thesis (M.D.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (p. 217-232). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web.

Tang, Ho Lam. / "December 2010." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 119-132). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

Song, Qingkun. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 144-157). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

by Ng Ping-chung. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1994. / Includes bibliographical references (leaves 161-179). / List of Abbreviation / Abstract / Acknowledgements / Table of contents / Chapter 1. --- Introduction / Chapter 1.1 --- Hormone and carcinogenesis --- p.1 / Chapter 1.2 --- Estrogen and carcinogenesis --- p.3 / Chapter 1.2.1 --- Carcinogenesis and endogenous sex hormone status --- p.3 / Chapter 1.2.2 --- Etiology of breast cancer --- p.3 / Chapter 1.2.2.1 --- Epidemiology --- p.3 / Chapter 1.2.2.2 --- Hormonal factors --- p.5 / Chapter 1.2.2.3 --- Genetic predisposition --- p.8 / Chapter 1.2.2.4 --- Influence of diet --- p.8 / Chapter 1.2.3 --- Hormonal therapy --- p.18 / Chapter 1.2.3.1 --- Anti-estrogen --- p.18 / Chapter 1.2.3.2 --- Progestins --- p.21 / Chapter 1.2.3.3 --- Aromatase inhibitor --- p.22 / Chapter 1.2.3.4 --- GnRH analogue therapy --- p.26 / Chapter 1.3 --- Estrogen pool --- p.26 / Chapter 1.4 --- Estrogen receptor --- p.30 / Chapter 1.4.1 --- General features of estrogen receptor and action mechanism --- p.30 / Chapter 1.4.2 --- Anti-estrogen binding site (AEBS) --- p.31 / Chapter 1.4.3 --- Physiological consideration --- p.32 / Chapter 1.4.3.1 --- Uterus: uterotrophic responses --- p.32 / Chapter 1.4.3.2 --- "Progesterone, the physiological estrogen antagonist" --- p.34 / Chapter 1.5 --- The role of growth factors and steroid hormones in breast cancer cell --- p.35 / Chapter 1.6 --- Alternate cytotoxic action of TAM --- p.37 / Chapter 1.7 --- In vitro models utilised in breast cancer study --- p.38 / Chapter 1.8 --- Current development of anti-estrogen --- p.39 / Chapter 1.9 --- Background about yuehchukene (YCK) --- p.41 / Chapter 2. --- Materials and methods / Chapter 2.1 --- Studies using whole animals --- p.47 / Chapter 2.1.1 --- Uterotrophic assay in rats --- p.47 / Chapter 2.1.2 --- Anti-implantation assay in rats --- p.48 / Chapter 2.1.3 --- Vaginal smear in mice --- p.49 / Chapter 2.2 --- Studies using breast cancer cells --- p.49 / Chapter 2.2.1 --- MCF-7 cell culture --- p.49 / Chapter 2.2.1.1 --- Measurement of cell number --- p.50 / Chapter 2.2.1.1.1 --- Cell count with haemocytometer --- p.50 / Chapter 2.2.1.1.2 --- Cell number estimated by DNA content in culture using Hoechst33258 --- p.51 / Chapter 2.2.1.1.3 --- Cell number estimated by [3H]-thymidine incorporation --- p.52 / Chapter 2.2.1.1.4 --- Preparation of dextran coated charcoal stripped serum --- p.52 / Chapter 2.2.2 --- MDA-MB-231 cell culture --- p.53 / Chapter 2.3 --- Studies using steroid receptors --- p.54 / Chapter 2.3.1 --- Rat uterine estrogen receptor --- p.54 / Chapter 2.3.2 --- Mice uterus and vaginal estrogen receptor --- p.55 / Chapter 2.3.3 --- MCF-7 cell estrogen receptor --- p.55 / Chapter 2.3.3.1 --- MCF-7 whole cell estrogen receptor binding --- p.55 / Chapter 2.3.3.2 --- Cytosolic estrogen receptor preparation from MCF-7 cell --- p.57 / Chapter 2.3.4 --- Progesterone receptor binding in MCF-7 cell --- p.57 / Chapter 2.3.5 --- Rat hepatic anti-estrogen binding site (AEBS) --- p.58 / Chapter 2.3.6 --- Estrogen receptor content estimation by enzyme immunoassay --- p.58 / Chapter 2.4 --- Enzyme studies related to estrogen metabolism --- p.60 / Chapter 2.4.1 --- Rat uterine ornithine decarboxylase (ODC) --- p.60 / Chapter 2.4.2 --- Rat hepatic ethoxyresorufin O-deethylase (EROD) --- p.60 / Chapter 2.4.3 --- Rat hepatic estradiol-2-hydroxylase --- p.62 / Chapter 2.4.4 --- MCF-7 cell estradiol-2-hydroxylase --- p.62 / Chapter 2.4.5 --- Human placental microsomal aromatase activity --- p.63 / Chapter 2.5 --- Enzymatic studies related to signal transduction --- p.64 / Chapter 2.5.1 --- Inhibition of Protein Kinase C activity of MCF-7 cell and protein phosphorylation --- p.64 / Chapter 2.5.2 --- Inhibition of calmodulin activation of cyclic nuleotide phosphodiesterase --- p.66 / Chapter 2.6 --- "Preparation of Pre-YCK, crude-YCK and post-YCK fractions" --- p.67 / Chapter 2.7 --- Preparation of Indole-3-carbinol acid condensation product (I3Ca) --- p.71 / Chapter 2.8 --- Studies on TCP series of YCK analogues --- p.71 / Chapter 2.9 --- List of test compounds --- p.75 / Chapter 2. 10 --- List of radio-ligands --- p.77 / Chapter 2.11 --- Miscellaneous reagents related to cell culture --- p.78 / Chapter 2.11.1 --- Culture medium --- p.78 / Chapter 2.11.2 --- Fetal calf serum --- p.78 / Chapter 2.11.3 --- Penicillin-streptomycin powder --- p.78 / Chapter 2.11.4 --- Phosphate buffer saline --- p.78 / Chapter 2.12 --- "Solvents, chemical and scintillants" --- p.78 / Chapter 3. --- Result / Chapter 3.1 --- Rat uterotrophic response with EE2 and YCK --- p.80 / Chapter 3.2 --- Mice vaginal cornification with estradiol (E2) and YCK --- p.83 / Chapter 3.3 --- Human breast cancer cell culture --- p.86 / Chapter 3.3.1 --- MCF-7 cell growth with YCK --- p.86 / Chapter 3.3.2 --- MCF-7 cell growth with YCK analogues and other related compounds --- p.91 / Chapter 3.3.3 --- MDA-MB-231 cell culture --- p.100 / Chapter 3.4 --- Receptor Binding --- p.100 / Chapter 3.4.1 --- Rat uterine estrogen receptor --- p.100 / Chapter 3.4.2 --- Mice uterine and vaginal estrogen receptor --- p.103 / Chapter 3.4.3 --- MCF-7 whole cell and cytosolic estrogen receptor --- p.103 / Chapter 3.4.4 --- MCF-7 cell progesterone receptor --- p.107 / Chapter 3.4.5 --- Rat hepatic anti-estrogen binding sites (AEBS) --- p.111 / Chapter 3.5 --- Enzyme activities related to estrogen metabolism --- p.111 / Chapter 3.5.1 --- Rat uterine ornithine decarboxylase (ODC) --- p.111 / Chapter 3.5.2 --- Rat hepatic estradiol-2-hydroxylase and ethoxyresorufin O-deethylase --- p.114 / Chapter 3.5.3 --- MCF-7 cell estradiol-2-hydroxylase --- p.121 / Chapter 3.5.4 --- Human placenta and MCF-7 cell aromatase --- p.126 / Chapter 3.6 --- Enzyme activities related to signal transduction --- p.126 / Chapter 3.6.1 --- Protein kinase C inhibition in vitro --- p.126 / Chapter 3.6.2 --- Calmodulin-dependent phosphodiesterase inhibitory actions in vitro --- p.131 / Chapter 3.7 --- Studies on TCP series of YCK analogues --- p.131 / Chapter 4. --- Discussion / Chapter 4.1 --- Estrogenicity of YCK --- p.140 / Chapter 4.2 --- Estrogenicity of YCK correlates with estrogen receptor (ER) binding --- p.141 / Chapter 4.3 --- Attenuation by YCK --- p.142 / Chapter 4.3.1 --- Attenuation by YCK on estrogen induced uterotrophic activity --- p.142 / Chapter 4.3.2 --- Attenuation by YCK on mice vaginal cornification with estradiol and YCK --- p.142 / Chapter 4.3.3 --- Attenuation by YCK on MCF-7 cell growth --- p.143 / Chapter 4.3.4 --- Attenuation of YCK on ornithine decarboxylase (ODC) induced by estrogen --- p.144 / Chapter 4.4 --- Deviation between YCK potency and RBA --- p.145 / Chapter 4.5 --- Estrogen inhibition action of YCK via non receptor binding mechanism --- p.148 / Chapter 4.6 --- Protein kinase C/ calmodulin-dependent phosphodiesterase inhibitor --- p.152 / Chapter 4.7 --- Progesterone receptor --- p.154 / Chapter 4.8 --- Aromatase inhibitor? --- p.155 / Chapter 4.9 --- Posssible mechanism for the attenuation of estrogenic action by YCK --- p.157 / Chapter 4.10 --- TCP series of YCK analogues --- p.158 / Chapter 4.11 --- Future works --- p.159 / Chapter 5. --- Reference --- p.161 / Appendix / Appendix 1 YCK analogues / Appendix 2 Structure of compounds mentioned in this thesis

Cheung Siu-king. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves [103-113]). / Abstracts in English and Chinese. / ACKNOWLEDGMENT --- p.i / TABLE OF CONTENTS --- p.ii / LIST OF ABBREVIATIONS --- p.vi / LIST OF TABLES --- p.vi / LIST OF FIGURES --- p.ix / ABSTRACT (ENGLISH VERSION) --- p.x / ABSTRACT (CHINESE VERSION) --- p.xii / Chapter 1. --- INTRODUCTION --- p.1 / Chapter 1.1. --- ADOLESCENT IDIOPATHIC SCOLIOSIS --- p.1 / Chapter 1.1.1. --- prevalence and geographic patterns of ais --- p.1 / Chapter 1.1.2. --- CLINICAL ASPECTS OF AIS --- p.3 / Chapter 1.1.3. --- ETIOLOGY OF AIS --- p.8 / Chapter 1.2. --- OBJECTIVES OF THIS STUDY --- p.24 / Chapter 2. --- SUBJECTS AND METHODS --- p.25 / Chapter 2.1. --- STUDY DESIGN --- p.25 / Chapter 2.2. --- SUBJECTS RECRUITMENT --- p.25 / Chapter 2.2.1. --- ais subjects --- p.25 / Chapter 2.2.2. --- control subjects --- p.25 / Chapter 2.2.3. --- GROUPING ACCORDING TO THE CHRONOLOGICAL AGE --- p.26 / Chapter 2.2.4. --- informed Consent --- p.26 / Chapter 2.2.5. --- EVALUATION OF COBB'S ANGLE --- p.26 / Chapter 2.3. --- ANTHROPOMETRIC ASSESSMENTS --- p.26 / Chapter 2.4. --- BMD MEASUREMENTS --- p.28 / Chapter 2.4.1. --- measured by dexa --- p.28 / Chapter 2.4.2. --- measured by pqct --- p.30 / Chapter 2.5. --- BONE FORMATION MARKER ： BALP --- p.32 / Chapter 2.5.1. --- SERUM COLLECTION --- p.32 / Chapter 2.5.2. --- ABBOTT METHODS FOR SERUM ALP ACTIVITY --- p.32 / Chapter 2.6. --- BONE RESORPTION MARKER ： DPD --- p.34 / Chapter 2.6.1. --- PYRILINK-D KITS REAGENT --- p.34 / Chapter 2.6.2. --- CREATININE ASSAY --- p.34 / Chapter 2.7. --- GENETIC MARKER - POLYMORPHISM OF ESTROGEN RECEPTOR GENE --- p.38 / Chapter 2.7.1. --- DIGESTION OF PERIPHERAL BLOOD CELLS --- p.38 / Chapter 2.7.2. --- QUANTITATION OF DNA --- p.39 / Chapter 2.7.3. --- CONFIRMATION OF INTEGRITY OF DNA --- p.39 / Chapter 2.7.4. --- POLYMERASE CHAIN REACTION (PCR) --- p.39 / Chapter 2.7.5. --- REACTION BUFFER --- p.39 / Chapter 2.8. --- STATISTICS --- p.45 / Chapter 3. --- RESULTS --- p.46 / Chapter 3 .1 --- SUBJECT DISTRIBUTION OF AIS AND NORMAL CONTROL --- p.46 / Chapter 3.1.1. --- "mean ages of menarche, breast development and pubic hair development" --- p.47 / Chapter 3.1.2. --- "PUBERTAL STATUES OF DIFFERENT AGE GROUPS EVALUATED BY MENARCHE, BREAST DEVELOPMENT AND PUBIC HAIR DEVELOPMENT" --- p.48 / Chapter 3.2. --- ANTHROPOMETRIC ASSESSMENTS --- p.49 / Chapter 3.2.1. --- OVERALL REVIEW OF ANTHROPOMETRIC ASSESSMENTS --- p.49 / Chapter 3.2.2. --- ANTHROPOMETRIC ASSESSMENTS ACCORDING TO THE CHRONOLOGICAL AGE --- p.50 / Chapter 3.3. --- BMD PROFILE OF AIS PATIENTS --- p.51 / Chapter 3.3.1. --- ABMD MEASURED BY DEXA (OVERALL REVIEW) --- p.51 / Chapter 3.3.2. --- ABMD IN DIFFERENT AGE GROUPS --- p.52 / Chapter 3.3.3. --- VBMD MEASURED BY PQCT (OVERALL REVIEW) --- p.52 / Chapter 3.3.4. --- VBMD IN DIFFERENT AGE GROUPS --- p.53 / Chapter 3.3.5. --- PREVALENCE OF OSTEOPENIA IN AIS PATIENTS --- p.53 / Chapter 3.3.6. --- SYMMETRY OF BILATERAL PROXIMAL FEMUR AND DISTAL TIBIA … --- p.54 / Chapter 3.3.7. --- CORRELATION OF ABMD AND VBMD WITH ANTHROPOMETRIC PARAMETERS AND SPINAL DEFORMITY --- p.54 / Chapter 3.4. --- BONE FORMATION MARKER- BALP --- p.55 / Chapter 3.5. --- BONE RESORPTION MARKER -DPD --- p.56 / Chapter 3.6. --- GENETIC MARKER -ESTROGEN RECEPTOR GENE --- p.57 / Chapter 4 --- DISCUSSION…… --- p.84 / Chapter 4.1 --- BONE MINERAL DENSITY OF AIS PATIENTS --- p.84 / Chapter 4.2 --- ANTHROPOMETRIC MEASUREMENTS --- p.89 / Chapter 4.3 --- BONE BIOCHEMICAL TURNOVER MARKER --- p.91 / Chapter 4.4 --- GENETIC MARKER - ER GENE --- p.97 / Chapter 4.4.1 --- OSTEOPORTIC CANDIDATE GENE- ER GENE --- p.98 / Chapter 4.4.2 --- NO CORRELATION BETWEEN ER GENE AND AIS --- p.99 / Chapter 4.5 --- SUMMARY --- p.100 / Chapter 5. --- CONCLUSION --- p.101 / BIBLIOGRAPHY --- p.XIV / APPENDIX --- p.XXV