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MPH, School of Public Health, Faculty of Health Sciences, University of the Witwatersrand, 2009 / Introduction: Cervical cancer is caused by persistent infection with high-risk Human Papilloma Virus (HPV) and is a leading cause of cancer deaths in South African women aged 15-65years. We estimated prevalence of abnormal (Atypical squmous cells of unknown significance to invasive cervical cancer) cervical cytology and associated cofactors in 18-35-year old women who tested negative for Human Immuno deficiency Virus (HIV). Method: This cervical lesion study was secondary analysis of data collected during a Microbicide Feasibility Study (MFS). MFS recruited 1100 women from public health care facilities. Women were interviewed and socio-demographic, sexual behaviour and clinical information was collected. If HIV negative, cervical and vaginal swabs were collected for Pap smear and laboratory testing for sexually-transmitted infections (STI). For the cervical lesion study, 808 women were eligible and 752 were enrolled in the study. Associations with abnormal cervical cytology were analysed using multiple logistic regression, and were reported as adjusted odds ratio (AOR) with a 95% confidence interval (CI). Results: We analysed 570 cytology specimens. Prevalence of abnormal cervical cytology was 6.7% (95% CI 4.8-9.0). Women who had an abnormal cervical cytology result were more likely than those with normal cytology results to report abnormal vaginal discharge (OR 2.33; 95% CI 1.07-5.06; p=0.03). They were also more likely to have more than one child (OR 2.21; 95% CI 1.00-4.87; p=0.05). v Discussion and conclusion: Our study showed that LSIL is common in this younger age group. Because HPV infection and thus abnormal cervical cytology are high among the younger population, this result is not unexpected. Since most LSIL regress naturally, our data support the current South African screening protocol for cervical cancer.

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The focus of this study was to explore women’s experiences with follow-up after an abnormal mammogram, and factors that influence follow-up. Factors, including health status, found in the cancer screening and treatment literature, are necessary in identifying variables which have the potential to affect a person’s perception, and promote or deter follow-up. Protection Motivation Theory constructs utilized in this study are found in the literature to improve diagnostic health behaviors such as performing breast self-examination and complying with diagnostic tests. A non-experimental, descriptive, cross-sectional design was used to identify the barriers to follow-up after an abnormal mammogram by: 1) determining the noncompliance rate of follow-up mammograms among women screened at an urban hospital’s mammography mobile unit in North Texas (October 1, 2004, to September 31, 2005) who were found to need further evaluation for suspected abnormal findings; and 2) identifying factors associated with noncompliance and perceived barriers to noncompliance. The sample consisted of 262 participants, 136 (52%) women whom the hospital reported had not returned for follow-up and 126 (48%) women who were reported to have returned. A logistic regression model was performed using follow-up as the dependent variable. The variables most related to follow-up were (1) number of mammograms in the last 5 years; (2) having health insurance; (3) having problems receiving abnormal mammogram results; (4) having problems receiving or making a follow-up appointment; (5) taking off from work for the follow-up appointment; (6) not having transportation to follow-up appointment; and (7) waiting a long time to receive the follow-up appointment. Non-compliance to recommended follow-up after an abnormal mammogram is a serious public health concern, since breast cancer screening can improve breast cancer outcomes only if prompt diagnostic resolution and access to state-of-the-art care is available to all screening participants. This study adds to the literature on predictors of follow-up after an abnormal mammogram, as well as the to the health disparities literature.

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Thesis (Ph. M.)--University of Wisconsin--Madison, 1937. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (Ph. M.)--University of Wisconsin--Madison, 1945. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (M.S.)--University of Wisconsin--Madison, 1944. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

No description available.

Hemoglobinopathies, the disorders of hemoglobin structure and synthesis, can be divided into two forms of clinical manifestation, namely thalassemias and abnormal hemoglobins. Thalassemia appears to involve an abnormal gene which results in a reduced rate of globin synthesis and it presents clinically as a hypochromic microcytic anemia. Its cause lies in some abnormality of the regulation of globin synthesis. An abnormal hemoglobin is usually the result of a mutation of one base in a codon triplet of the structural gene for one or other hemoglobin chain which leads to an amino acid substitution in the primary structure of the globin. In this study, the biochemical characterization of five samples of abnormal hemoglobin which were obtained from patients at Vancouver General Hospital, Vancouver, B.C. and Siriraj Hospital, Bangkok is described. In the first case from V.G.H., the propositus, a 17 month old Chinese girl showed a fast (anionic) abnormal hemoglobin from birth. In a biochemical investigation of the variant from her father it was found that the glycine residue 56 in the β-chain was substituted by aspartic acid. This mutant is identical to that previously designated as HbJ Bangkok ([formula omitted]). The second case, a 21 year old Thai male in Bangkok was shown to be a double heterozygote with both a slow and a fast abnormal hemoglobin and an absence of HbA upon starch gel electrophoresis. Structural characterization of the separated globin chain of both variants indicated that the mutation in the slow variant occurred at residue 26 of β-chain where glutamic acid was replaced by lysine. This mutation is similar to that previously described as HbE ([formula omitted]). The fast variant showed an amino acid alteration at position 113 of β-chain where valine was substituted by glutamic acid. This mutation is identical with Hb New York ([formula omitted]). A double heterozygote involving both HbE and Hb New York has not been previously described. The other three samples from unrelated patients in Bangkok revealed a slow mutant on starch gel electrophoresis and biochemical studies showed that residue 74 in the α-chain was changed from an aspartyl to a histidyl residue. This mutation has not been previously described. It is proposed that this new hemoglobin ([formula omitted]) be called Hb Mahidol after Mahidol University in Bangkok. In one of the three patients showing Hb Mahidol interaction with α-thalassemia (α-thalassemia-Hb Mahidol) occurs. This results in the clinical features of chronic hemolytic anemia and a total absence of HbA which is replaced by Hb Mahidol together with some HbH([formula omitted]). / Medicine, Faculty of / Pathology and Laboratory Medicine, Department of / Graduate