Browsing by Author "Asiimwe, Edgar"

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    Educational Attainment and Personal Willingness to Undergo Safe Male Circumcision Among Young Men in Rural Uganda.
    (2011) Asiimwe, Edgar

    Previous models have demonstrated that high uptake of male circumcision (MC) will be required if the procedure is to have a significant public health impact in sub-Saharan African countries (Nagelkerke et al., 2007). Therefore, research about the determinants of uptake of MC among different groups is warranted. The objective of this study was to examine the relationship between educational attainment and personal willingness to undergo safe male circumcision (SMC) in rural Uganda.

    In this study, we surveyed 297 participants (aged 18-24) in three rural districts. Additionally, we conducted focus group discussions with between 8-12 participants in each of these districts.

    We found that circumcision prevalence and characteristics of those who are circumcised were similar to findings shown elsewhere. Additionally, we found that personal willingness to undergo SMC was lower among respondents with higher educational attainment [OR (crude) = 0.28; p=0.002; CI: 0.12-0.62]. This odds ratio remained statistically significant when we adjusted for demographic confounders [OR = 0.20; p=0.001; CI: 0.08-0.52]. We did not observe any significant difference in willingness between those who had no educational attainment and those who had completed primary education only [OR= 0.90; p=0.89; CI: 0.22-3.68].

    We conclude that young men with higher education are less willing to undergo SMC than their less educated peers. In addition, our qualitative results indicate that inadequate information about SMC, among those with higher education, might explain this difference in willingness to undergo the procedure.

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    Stratified whole genome linkage analysis of Chiari type I malformation implicates known Klippel-Feil syndrome genes as putative disease candidates.
    (PloS one, 2013-01) Markunas, Christina A; Soldano, Karen; Dunlap, Kaitlyn; Cope, Heidi; Asiimwe, Edgar; Stajich, Jeffrey; Enterline, David; Grant, Gerald; Fuchs, Herbert; Gregory, Simon G; Ashley-Koch, Allison E
    Chiari Type I Malformation (CMI) is characterized by displacement of the cerebellar tonsils below the base of the skull, resulting in significant neurologic morbidity. Although multiple lines of evidence support a genetic contribution to disease, no genes have been identified. We therefore conducted the largest whole genome linkage screen to date using 367 individuals from 66 families with at least two individuals presenting with nonsyndromic CMI with or without syringomyelia. Initial findings across all 66 families showed minimal evidence for linkage due to suspected genetic heterogeneity. In order to improve power to localize susceptibility genes, stratified linkage analyses were performed using clinical criteria to differentiate families based on etiologic factors. Families were stratified on the presence or absence of clinical features associated with connective tissue disorders (CTDs) since CMI and CTDs frequently co-occur and it has been proposed that CMI patients with CTDs represent a distinct class of patients with a different underlying disease mechanism. Stratified linkage analyses resulted in a marked increase in evidence of linkage to multiple genomic regions consistent with reduced genetic heterogeneity. Of particular interest were two regions (Chr8, Max LOD = 3.04; Chr12, Max LOD = 2.09) identified within the subset of "CTD-negative" families, both of which harbor growth differentiation factors (GDF6, GDF3) implicated in the development of Klippel-Feil syndrome (KFS). Interestingly, roughly 3-5% of CMI patients are diagnosed with KFS. In order to investigate the possibility that CMI and KFS are allelic, GDF3 and GDF6 were sequenced leading to the identification of a previously known KFS missense mutation and potential regulatory variants in GDF6. This study has demonstrated the value of reducing genetic heterogeneity by clinical stratification implicating several convincing biological candidates and further supporting the hypothesis that multiple, distinct mechanisms are responsible for CMI.