The Histopathology Core will be responsible for supporting all the histological, immunocytochemical, and in situ hybridization methodology for three research projects in this application. The histological analysis of a skeletal tissue provides a unique challenge due to its mineralized nature and virtual impenetrability to stains, antibodies, and probes. Thus, the dedication of an independent core unit under the direction of an experienced pathologist is of paramount importance for the completion of the proposed work. Described within this Core, outlined are the methods and pitfalls associated with working with skeletal tissues as well as a comprehensive bibliography demonstrating the ability of the staff to solve problems in the analyses of the tissues. All expenses related to tissue and cell processing for the 3 research projects will be administered through the Histopathology Core.

Agency
National Institute of Health (NIH)
Institute
National Institute of Environmental Health Sciences (NIEHS)
Type
Research Program Projects (P01)
Project #
1P01ES011854-01
Application #
6571141
Study Section
Special Emphasis Panel (ZES1)
Project Start
2002-07-01
Project End
2006-06-30
Budget Start
Budget End
Support Year
1
Fiscal Year
2002
Total Cost
Indirect Cost
Name
University of Rochester
Department
Type
DUNS #
208469486
City
Rochester
State
NY
Country
United States
Zip Code
14627
Beier, Eric E; Holz, Jonathan D; Sheu, Tzong-Jen et al. (2016) Elevated Lifetime Lead Exposure Impedes Osteoclast Activity and Produces an Increase in Bone Mass in Adolescent Mice. Toxicol Sci 149:277-88
Shu, Lei; Beier, Eric; Sheu, Tzong et al. (2015) High-fat diet causes bone loss in young mice by promoting osteoclastogenesis through alteration of the bone marrow environment. Calcif Tissue Int 96:313-23
Beier, Eric E; Inzana, Jason A; Sheu, Tzong-Jen et al. (2015) Effects of Combined Exposure to Lead and High-Fat Diet on Bone Quality in Juvenile Male Mice. Environ Health Perspect 123:935-43
Beier, Eric E; Sheu, Tzong-Jen; Dang, Deborah et al. (2015) Heavy Metal Ion Regulation of Gene Expression: MECHANISMS BY WHICH LEAD INHIBITS OSTEOBLASTIC BONE-FORMING ACTIVITY THROUGH MODULATION OF THE Wnt/?-CATENIN SIGNALING PATHWAY. J Biol Chem 290:18216-26
Beier, Eric E; Sheu, Tzong-Jen; Buckley, Taylor et al. (2014) Inhibition of beta-catenin signaling by Pb leads to incomplete fracture healing. J Orthop Res 32:1397-405
Beier, Eric E; Maher, Jason R; Sheu, Tzong-Jen et al. (2013) Heavy metal lead exposure, osteoporotic-like phenotype in an animal model, and depression of Wnt signaling. Environ Health Perspect 121:97-104
Holz, Jonathan D; Beier, Eric; Sheu, Tzong-Jen et al. (2012) Lead induces an osteoarthritis-like phenotype in articular chondrocytes through disruption of TGF-? signaling. J Orthop Res 30:1760-6
van Wijngaarden, Edwin; Campbell, James R; Cory-Slechta, Deborah A (2009) Bone lead levels are associated with measures of memory impairment in older adults. Neurotoxicology 30:572-80
Zuscik, Michael J; Ma, Lin; Buckley, Taylor et al. (2007) Lead induces chondrogenesis and alters transforming growth factor-beta and bone morphogenetic protein signaling in mesenchymal cell populations. Environ Health Perspect 115:1276-82
Awad, Hani A; Zhang, Xinping; Reynolds, David G et al. (2007) Recent advances in gene delivery for structural bone allografts. Tissue Eng 13:1973-85

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