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Item Differential effects of Epigallocatechin-3-gallate containing supplements on correcting skeletal defects in a Down syndrome mouse model(Wiley, 2016-04) Abeysekera, Irushi; Thomas, Jared; Georgiadis, Taxiarchis M.; Berman, Alycia G.; Hammond, Max A.; Dria, Karl J.; Wallace, Joseph M.; Roper, Randall J.; Biology, School of ScienceSCOPE: Down syndrome (DS), caused by trisomy of human chromosome 21 (Hsa21), is characterized by a spectrum of phenotypes including skeletal abnormalities. The Ts65Dn DS mouse model exhibits similar skeletal phenotypes as humans with DS. DYRK1A, a kinase encoded on Hsa21, has been linked to deficiencies in bone homeostasis in DS mice and individuals with DS. Treatment with Epigallocatechin-3-gallate (EGCG), a known inhibitor of Dyrk1a, improves some skeletal abnormalities associated with DS in mice. EGCG supplements are widely available but the effectiveness of different EGCG-containing supplements has not been well studied. METHODS AND RESULTS: Six commercially available supplements containing EGCG were analyzed, and two of these supplements were compared with pure EGCG for their impact on skeletal deficits in a DS mouse model. The results demonstrate differential effects of commercial supplements on correcting skeletal abnormalities in Ts65Dn mice. Different EGCG-containing supplements display differences in degradation, polyphenol content, and effects on trisomic bone. CONCLUSION: This work suggests that the dose of EGCG and composition of EGCG-containing supplements may be important in correcting skeletal deficits associated with DS. Careful analyses of these parameters may lead to a better understanding of how to improve skeletal and other deficits that impair individuals with DS.Item Genetically predicted circulating concentrations of micronutrients and risk of colorectal cancer among individuals of European descent: a Mendelian randomization study(Elsevier, 2021) Tsilidis, Konstantinos K.; Papadimitriou, Nikos; Dimou, Niki; Gill, Dipender; Lewis, Sarah J.; Martin, Richard M.; Murphy, Neil; Markozannes, Georgios; Zuber, Verena; Cross, Amanda J.; Burrows, Kimberley; Lopez, David S.; Key, Timothy J.; Travis, Ruth C.; Perez-Cornago, Aurora; Hunter, David J.; van Duijnhoven, Fränzel J. B.; Albanes, Demetrius; Arndt, Volker; Berndt, Sonja I.; Bézieau, Stéphane; Bishop, D. Timothy; Boehm, Juergen; Brenner, Hermann; Burnett-Hartman, Andrea; Campbell, Peter T.; Casey, Graham; Castellví-Bel, Sergi; Chan, Andrew T.; Chang-Claude, Jenny; de la Chapelle, Albert; Figueiredo, Jane C.; Gallinger, Steven J.; Giles, Graham G.; Goodman, Phyllis J.; Gsur, Andrea; Hampe, Jochen; Hampel, Heather; Hoffmeister, Michael; Jenkins, Mark A.; Keku, Temitope O.; Kweon, Sun-Seog; Larsson, Susanna C.; Le Marchand, Loic; Li, Christopher I.; Li, Li; Lindblom, Annika; Martín, Vicente; Milne, Roger L.; Moreno, Victor; Nan, Hongmei; Nassir, Rami; Newcomb, Polly A.; Offit, Kenneth; Pharoah, Paul D. P.; Platz, Elizabeth A.; Potter, John D.; Qi, Lihong; Rennert, Gad; Sakoda, Lori C.; Schafmayer, Clemens; Slattery, Martha L.; Snetselaar, Linda; Schenk, Jeanette; Thibodeau, Stephen N.; Ulrich, Cornelia M.; Van Guelpen, Bethany; Harlid, Sophia; Visvanathan, Kala; Vodickova, Ludmila; Wang, Hansong; White, Emily; Wolk, Alicja; Woods, Michael O.; Wu, Anna H.; Zheng, Wei; Bueno-de-Mesquita, Bas; Boutron-Ruault, Marie-Christine; Hughes, David J.; Jakszyn, Paula; Kühn, Tilman; Palli, Domenico; Riboli, Elio; Giovannucci, Edward L.; Banbury, Barbara L.; Gruber, Stephen B.; Peters, Ulrike; Gunter, Marc J.; Epidemiology, School of Public HealthBackground: The literature on associations of circulating concentrations of minerals and vitamins with risk of colorectal cancer is limited and inconsistent. Evidence from randomized controlled trials (RCTs) to support the efficacy of dietary modification or nutrient supplementation for colorectal cancer prevention is also limited. Objectives: To complement observational and RCT findings, we investigated associations of genetically predicted concentrations of 11 micronutrients (β-carotene, calcium, copper, folate, iron, magnesium, phosphorus, selenium, vitamin B-6, vitamin B-12, and zinc) with colorectal cancer risk using Mendelian randomization (MR). Methods: Two-sample MR was conducted using 58,221 individuals with colorectal cancer and 67,694 controls from the Genetics and Epidemiology of Colorectal Cancer Consortium, Colorectal Cancer Transdisciplinary Study, and Colon Cancer Family Registry. Inverse variance-weighted MR analyses were performed with sensitivity analyses to assess the impact of potential violations of MR assumptions. Results: Nominally significant associations were noted for genetically predicted iron concentration and higher risk of colon cancer [ORs per SD (ORSD): 1.08; 95% CI: 1.00, 1.17; P value = 0.05] and similarly for proximal colon cancer, and for vitamin B-12 concentration and higher risk of colorectal cancer (ORSD: 1.12; 95% CI: 1.03, 1.21; P value = 0.01) and similarly for colon cancer. A nominally significant association was also noted for genetically predicted selenium concentration and lower risk of colon cancer (ORSD: 0.98; 95% CI: 0.96, 1.00; P value = 0.05) and similarly for distal colon cancer. These associations were robust to sensitivity analyses. Nominally significant inverse associations were observed for zinc and risk of colorectal and distal colon cancers, but sensitivity analyses could not be performed. None of these findings survived correction for multiple testing. Genetically predicted concentrations of β-carotene, calcium, copper, folate, magnesium, phosphorus, and vitamin B-6 were not associated with disease risk. Conclusions: These results suggest possible causal associations of circulating iron and vitamin B-12 (positively) and selenium (inversely) with risk of colon cancer.