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Dale L. Goad

Researcher at Harvard University

Publications -  7
Citations -  872

Dale L. Goad is an academic researcher from Harvard University. The author has contributed to research in topics: Resorption & Prostaglandin E2. The author has an hindex of 7, co-authored 7 publications receiving 850 citations.

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PTHrP and Indian hedgehog control differentiation of growth plate chondrocytes at multiple steps.

TL;DR: It is suggested that Indian hedgehog positively controls differentiation of periarticular chondrocytes independently of PTHrP, which indicates that chONDrocyte differentiation is controlled at multiple steps by P THrP and Ihh through the mutual regulation of their activities.
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Enhanced expression of vascular endothelial growth factor in human SaOS-2 osteoblast-like cells and murine osteoblasts induced by insulin-like growth factor I.

TL;DR: Testing the hypothesis that insulin-like growth factor I (IGF-I), a known osteogenic factor, modulates VEGF expression in osteoblasts concludes that IGF-I enhances osteoblast synthesis of V EGF, which may then act locally on endothelium to stimulate angiogenesis, an essential component of bone growth and remodeling.
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Tumor Necrosis Factor-α (Cachectin) Stimulates Bone Resorption in Mouse Calvaria via a Prostaglandin-Mediated Mechanism

TL;DR: The findings indicate that a host factor produced in response to malignant cells can cause enhanced bone resorption, and the concept of the humoral hypercalcemias of malignancy must be expanded to include mediators not produced by the tumor cells themselves.
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Human Parathyroid Hormone (PTH)-Related Protein and Human PTH: Comparative Biological Activities on Human Bone Cells and Bone Resorption

TL;DR: HPTHrP-(1-34) and hPTH-related protein have similar high specific biological activities to stimulate production of cAMP in human osteoblast-like cells, but that hP THrP-1- 34 is modestly less potent to stimulate bone resorption in mouse calvariae.
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Insulin-like growth factor-I inhibits parathyroid hormone-stimulated and enhances prostaglandin E2-stimulated adenosine 3',5'-monophosphate production by human osteoblast-like SaOS-2 cells.

TL;DR: It is found that physiologically relevant concentrations of IGF-I specifically inhibited PTH-stimulated and enhanced PGE2- Stimulated production of cAMP by an action at the level of PTH and P GE2 receptors and/or coupling of the receptors to Gs alpha.