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Summary: PURPOSE: The purpose of this study was to compare relationships between dietary and physical activity (PA) behaviors and body composition and body fat distribution, as measured by percent body fat (BF%), waist-to-height ratio (WHt), waistto- hip ratio (WHp) and body mass index (BMI) in post-menopausal women (Post), with the same relationships in pre-menopausal women (Pre). METHODS: Ninety-two subjects (n = 48 Post; n = 44 Pre) were measured for height, weight, waist and hip circumferences and skinfold thicknesses. Dietary content was obtained from a Diet History Questionnaire (DHQ II); PA was estimated from responses to the International Physical Activity Questionnaire (IPAQ). RESULTS: Multiple regression identified no modifiable predictor variables for Pre. Models for Post identified saturated fat grams (SFGs), PA, years postmenopause (YrsPost), and Alcohol (Alc) as predictors of WHt, WHp, BMI and BF%. CONCLUSIONS: PA, SFG and Alc are modifiable variables related to postmenopausal body composition and fat distribution., 2017, Includes bibliography., Degree granted: Thesis (M.S.)--Florida Atlantic University, 2017., Collection: FAU Electronic Theses and Dissertations Collection

The heritability of B cell chronic lymphocytic leukemia (CLL) is relatively high; however, no predisposing mutation has been convincingly identified. We show that loss or reduced expression of death-associated protein kinase 1 (DAPK1) underlies cases of heritable predisposition to CLL and the majority of sporadic CLL. Epigenetic silencing of DAPK1 by promoter methylation occurs in almost all sporadic CLL cases. Furthermore, we defined a disease haplotype, which segregates with the CLL phenotype in a large family. DAPK1 expression of the CLL allele is downregulated by 75% in germline cells due to increased HOXB7 binding. In the blood cells from affected family members, promoter methylation results in additional loss of DAPK1 expression. Thus, reduced expression of DAPK1 can result from germline predisposition, as well as epigenetic or somatic events causing or contributing to the CLL phenotype.