Objectives The predictive capabilities of skinfold regression equations are limited across populations and current equations may not be well suited for the prediction of body fat in older adults or obese Americans. The goal of this study was to compare percent body fat (%BF) predicted by several skinfold regression equations to %BF determined by Dual-Energy X-ray Absorptiometry (DXA) in obese and non-obese Caucasian men and women in the United states over the age of 65 years. Design A block design was used with two blocks: obesity (non-obese/obese) and gender (male/female). All subjects underwent the same testing procedures in one visit. Setting University of Pittsburgh Clinical and Translation Research Center. Participants Seventy-eight older healthy adults were recruited for participation. Measurements Actual percent body fat was determined from a whole body DXA scan. Estimated percent body fat (%BF) was calculated using skinfold measurements and established regression equations. The predictive accuracy of the regression equations was evaluated by comparing the estimated %BF to the actual %BF measured with DXA using a within subject ANOVA (α=0.05). This was done within subgroups: obese males, obese females, non-obese males and non-obese females. Results Durnin and Womersly and Jackson and Pollock had reasonably good agreement with DXA in older Caucasian American females and males, respectively. The remaining equations significantly overestimated %BF in older Caucasian American males. Mixed results were found in females with Gause-Nilsson and Jackson and Pollock significantly underestimating %BF, while Visser and Kwok overestimated %BF. Conclusion Numerous factors of a population including age, race, ethnicity, gender and obesity should be considered when selecting a skinfold regression equation to estimate %BF. While Durnin and Womersly and Jackson and Pollock are recommended for predicting %BF in older Caucasian American females and males, respectively, there exists a need to develop accurate regression models that consider obesity, gender, race or ethnicity when predicting %BF in a diverse geriatric American population.
Overexpression of the NEDD9/HEF1/Cas-L scaffolding protein is frequent, and drives invasion and metastasis in breast, head and neck, colorectal, melanoma, lung, and other types of cancer. We have examined the consequences of genetic ablation of Nedd9 in the MMTV-HER2/ERBB2/neu mouse mammary tumor model. Unexpectedly, we found that only a limited effect on metastasis in MMTV-neu;Nedd9−/− mice compared to MMTV-neu;Nedd9+/+ mice, but instead a dramatic reduction in tumor incidence (18% versus 80%), and a significantly increased latency until tumor appearance. Orthotopic reinjection and tail vein injection of cells arising from tumors, coupled with in vivo analysis, indicated tumors arising in MMTV-neu;Nedd9−/− mice had undergone mutational selection that overcame the initial requirement for Nedd9. To better understand the defects in early tumor growth, we compared mammary progenitor cell pools from MMTV-neu;Nedd9−/− versus MMTV-neu;Nedd9+/+ mice. The MMTV-neu;Nedd9−/− genotype selectively reduced both the number and colony-forming potential of mammary luminal epithelial progenitor cells, while not affecting basal epithelial progenitors. MMTV-neu;Nedd9−/−mammospheres had striking defects in morphology and cell polarity. All of these defects were seen predominantly in the context of the HER2/neu oncogene, and were not associated with randomization of the plane of mitotic division, but rather with depressed expression the cell attachment protein FAK, accompanied by increased sensitivity to small molecule inhibitors of FAK and SRC. Surprisingly, in spite of these significant differences, only minimal changes were observed in the gene expression profile of Nedd9−/− mice, indicating critical Nedd9-dependent differences in cell growth properties were mediated via post-transcriptional regulation of cell signaling. Coupled with emerging data indicating a role for NEDD9 in progenitor cell populations during the morphogenesis of other tissues, these results indicate a functional requirement for NEDD9 in the growth of mammary cancer progenitor cells.
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