Robert D. Ward
University of Michigan
6 Papers
234 Citations
Robert D. Ward is an academic researcher from University of Michigan. The author has contributed to research in topics: Pituitary gland & Thyrotropic cell. The author has an hindex of 6, co-authored 6 publications. Previous affiliations of Robert D. Ward include Baylor College of Medicine.
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Papers
Pituitary hypoplasia and respiratory distress syndrome in Prop1 knockout mice
Igor O. Nasonkin,Robert D. Ward,Lori T. Raetzman,Audrey F. Seasholtz,Thomas L. Saunders,Patrick J. Gillespie,Patrick J. Gillespie,Sally A. Camper +7 more
TL;DR: It is shown that deletion of Prop1 in mice causes severe pituitary hypoplasia with failure of the entire Pit1 lineage and delayed gonadotrope development and Prop1-null mice are an excellent model for MPHD and may be useful for testing the efficacy of pharmaceutical intervention for neonatal respiratory distress.
Cell proliferation and vascularization in mouse models of pituitary hormone deficiency
TL;DR: The authors performed histological analysis of Pit1-and Prop1-deficient dwarf mouse pituitaries throughout fetal and postnatal development, and found that Pit1deficient mice first exhibit pituitary hypoplasia after birth, primarily caused by reduced cell proliferation, although there is some apoptosis.
Comparative genomics reveals functional transcriptional control sequences in the Prop1 gene.
Robert D. Ward,Robert D. Ward,Shannon W. Davis,Min Chul Cho,Constance Esposito,Robert H. Lyons,Jan Fang Cheng,Edward M. Rubin,Simon J. Rhodes,Lori T. Raetzman,Lori T. Raetzman,Timothy P. L. Smith,Sally A. Camper +12 more
TL;DR: The usefulness of a comparative genomics approach in the identification of regulatory elements that may be the site of mutations responsible for some cases of MPHD is illustrated.
Aged PROP1 deficient dwarf mice maintain ACTH production.
Igor O. Nasonkin,Robert D. Ward,David L. Bavers,Felix Beuschlein,Amanda H. Mortensen,Catherine E. Keegan,Gary D. Hammer,Sally A. Camper +7 more
TL;DR: It is suggested that the mouse model differs from the human patients who display progressive hormone loss and hypocortisolism, and young adult Prop1 deficient mice are capable of responding to restraint stress with further elevation of ACTH and corticosterone.