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Demographic and lifestyle factors and selenium levels in men and women in the U.S.
Park, Kyong,Rimm, Eric,Siscovick, David,Spiegelman, Donna,Morris, J. Steven,Mozaffarian, Dariush The Korean Nutrition Society 2011 Nutrition Research and Practice Vol. No.
Selenium is an antioxidant trace element linked to cardiovascular disease and cancer. Although diet is a major source, relatively little else is known about independent determinants of selenium levels in free-living humans. In this study, we aimed to investigate the independent demographic. lifestyle, and dietary determinants of selenium levels in 1,997 men and 1,905 women in two large prospective U.S. cohorts. Toenail selenium levels were quantified using neutron activation analysis. Diet, geographic residence, demographic, and environmental factors were assessed by validated self-administered questionnaires. Multivariate generalized linear models were conducted to assess the independent relations of these factors with toenail selenium levels, correcting for measurement error in the diet. In multi variable-adjusted analyses, independent predictors of higher selenium were male gender (6.3% higher levels); living in West and Northern-Midwest U.S. regions (8.9% and 7.4% higher than Southern-Midwest regions, respectively); consumption of beef and bread products (between 0.7 - 2.5% higher per daily serving); and selenium supplement use (6.9% higher than non-users); whereas cigarette smoking (5-10% lower than never smokers), older age (0.6% lower per 5 years), and consumption of eggs, white rice, dairy products, coffee, and alcohol (between 0.1 to 2.0% lower per daily serving) were associated with lower selenium. Multiple dietary and non-dietary factors independently predicted selenium levels, suggesting that both consumption and non-dietary processes (e.g.. related to oxidant status) may affect levels. Significant geographic variation in selenium levels exists in the US.
Demographic and lifestyle factors and selenium levels in men and women in the U.S.
Kyong Park,Eric Rimm,David Siscovick,Donna Spiegelman,J. Steven Morris,Dariush Mozaffarian 한국영양학회 2011 Nutrition Research and Practice Vol.5 No.4
Selenium is an antioxidant trace element linked to cardiovascular disease and cancer. Although diet is a major source, relatively little else is known about independent determinants of selenium levels in free-living humans. In this study, we aimed to investigate the independent demographic, lifestyle, and dietary determinants of selenium levels in 1,997 men and 1,905 women in two large prospective U.S. cohorts. Toenail selenium levels were quantified using neutron activation analysis. Diet, geographic residence, demographic, and environmental factors were assessed by validated self-administered questionnaires. Multivariate generalized linear models were conducted to assess the independent relations of these factors with toenail selenium levels, correcting for measurement error in the diet. In multivariable-adjusted analyses, independent predictors of higher selenium were male gender (6.3% higher levels); living in West and Northern-Midwest U.S. regions (8.9% and 7.4% higher than Southern-Midwest regions, respectively); consumption of beef and bread products (between 0.7 - 2.5% higher per daily serving); and selenium supplement use (6.9% higher than non-users); whereas cigarette smoking (5-10% lower than never smokers) , older age (0.6% lower per 5 years), and consumption of eggs, white rice, dairy products, coffee, and alcohol (between 0.1 to 2.0% lower per daily serving) were associated with lower selenium. Multiple dietary and non-dietary factors independently predicted selenium levels, suggesting that both consumption and non-dietary processes (e.g., related to oxidant status) may affect levels. Significant geographic variation in selenium levels exists in the US.
Park, Eun Sug,Hopke, Philip K.,Oh, Man-Suk,Symanski, Elaine,Han, Daikwon,Spiegelman, Clifford H. Oxford University Press 2014 Biostatistics Vol.15 No.3
<P>There has been increasing interest in assessing health effects associated with multiple air pollutants emitted by specific sources. A major difficulty with achieving this goal is that the pollution source profiles are unknown and source-specific exposures cannot be measured directly; rather, they need to be estimated by decomposing ambient measurements of multiple air pollutants. This estimation process, called multivariate receptor modeling, is challenging because of the unknown number of sources and unknown identifiability conditions (model uncertainty). The uncertainty in source-specific exposures (source contributions) as well as uncertainty in the number of major pollution sources and identifiability conditions have been largely ignored in previous studies. A multipollutant approach that can deal with model uncertainty in multivariate receptor models while simultaneously accounting for parameter uncertainty in estimated source-specific exposures in assessment of source-specific health effects is presented in this paper. The methods are applied to daily ambient air measurements of the chemical composition of fine particulate matter ([Formula]), weather data, and counts of cardiovascular deaths from 1995 to 1997 for Phoenix, AZ, USA. Our approach for evaluating source-specific health effects yields not only estimates of source contributions along with their uncertainties and associated health effects estimates but also estimates of model uncertainty (posterior model probabilities) that have been ignored in previous studies. The results from our methods agreed in general with those from the previously conducted workshop/studies on the source apportionment of PM health effects in terms of number of major contributing sources, estimated source profiles, and contributions. However, some of the adverse source-specific health effects identified in the previous studies were not statistically significant in our analysis, which probably resulted because we incorporated parameter uncertainty in estimated source contributions that has been ignored in the previous studies into the estimation of health effects parameters.</P>
TAZ, a Transcriptional Modulator of Mesenchymal Stem Cell Differentiation
Hong, Jeong-Ho,Hwang, Eun-Sook,McManus, Michael T.,Amsterdam, Adam,Tian, Yu,Kalmukova, Ralitsa,Mueller, Elisabetta,Benjamin, Thomas,Spiegelman, Bruce M.,Sharp, Phillip A.,Hopkins, Nancy,Yaffe, Michael 이화여자대학교 약학연구소 2005 藥學硏究論文集 Vol.- No.16
Mesenchymal stem celts (MSCs) are a pluripotent cell type that can differentiate into several distinct lineages. Two key transcription factors, Runx2 and peroxisome protiferator-activated receptor γ(PPARγ), drive MSCs to differentiate into either osteoblasts or adipocytes, respectively. How these two transcription factors are regulated in order to specify these alternate cell fates remains a pivotal question. Here we report that a 14-3-3-binding protein, TAZ(transcrip-tional coactivator with PDZ-binding motif), coactivates RunxB-dependent gene transcription while repressing PPARγ-dependent gene transcription. By modulating TAZ expression in model cell lines, mouse embryonic fibroblasts, and primary MSCs in culture and in zebrafish in vivo, we observed alterations in osteogenic versus adipogenic potential. These results indicate that TAZ functions as a molecular rheostat that modulates MSC differentiation.
Thrap3 docks on phosphoserine 273 of PPARγ and controls diabetic gene programming
Choi, Jang Hyun,Choi, Sun-Sil,Kim, Eun Sun,Jedrychowski, Mark P.,Yang, Yong Ryoul,Jang, Hyun-Jun,Suh, Pann-Ghill,Banks, Alexander S.,Gygi, Steven P.,Spiegelman, Bruce M. Cold Spring Harbor Laboratory Press 2014 Genes & development Vol.28 No.21
<P>Phosphorylation of PPARγ at Ser273 by cyclin-dependent kinase 5 (CDK5) in adipose tissue stimulates insulin resistance. Choi et al. find that Thrap3 (thyroid hormone receptor-associated protein 3) can directly interact with PPARγ when it is phosphorylated at Ser273, and this interaction controls the diabetic gene programing mediated by the phosphorylation of PPARγ. Reduced expression of Thrap3 in fat tissue by antisense oligonucleotides improves hyperglycemia and insulin resistance in high-fat-fed mice without affecting body weight.</P><P>Phosphorylation of peroxisome proliferator-activated receptor γ (PPARγ) at Ser273 by cyclin-dependent kinase 5 (CDK5) in adipose tissue stimulates insulin resistance, but the underlying molecular mechanisms are unclear. We show here that Thrap3 (thyroid hormone receptor-associated protein 3) can directly interact with PPARγ when it is phosphorylated at Ser273, and this interaction controls the diabetic gene programming mediated by the phosphorylation of PPARγ. Knockdown of Thrap3 restores most of the genes dysregulated by CDK5 action on PPARγ in cultured adipocytes. Importantly, reduced expression of Thrap3 in fat tissue by antisense oligonucleotides (ASOs) regulates a specific set of genes, including the key adipokines adiponectin and adipsin, and effectively improves hyperglycemia and insulin resistance in high-fat-fed mice without affecting body weight. These data indicate that Thrap3 plays a crucial role in controlling diabetic gene programming and may provide opportunities for the development of new therapeutics for obesity and type 2 diabetes.</P>