J
Joan C. Marini
Researcher at National Institutes of Health
Publications - 172
Citations - 9680
Joan C. Marini is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Osteogenesis imperfecta & Type I collagen. The author has an hindex of 49, co-authored 162 publications receiving 8762 citations. Previous affiliations of Joan C. Marini include Johns Hopkins University School of Medicine & Johns Hopkins University.
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Nanoscale morphology of Type I collagen is altered in the Brtl mouse model of Osteogenesis Imperfecta
TL;DR: Observations at the nanoscale level provide insight into the structural basis for changes present in bone composition, geometry and mechanical integrity in Brtl/+ bones, and further studies are necessary to link these morphological observations to nanoscales mechanical integrity.
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Osteogenesis imperfecta type IV. Detection of a point mutation in one alpha 1(I) collagen allele (COL1A1) by RNA/RNA hybrid analysis.
TL;DR: The finding of a glycine substitution in an alpha 1(I) chain of a patient with the milder type IV osteogenesis imperfecta phenotype requires modification of current molecular models for types II and IV osteogenic imperfecta.
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Alendronate treatment of the brtl osteogenesis imperfecta mouse improves femoral geometry and load response before fracture but decreases predicted material properties and has detrimental effects on osteoblasts and bone formation.
Thomas E Uveges,Kenneth M. Kozloff,Jennifer M. Ty,Jennifer M. Ty,Felicia Ledgard,Cathleen L. Raggio,Gloria Gronowicz,Steven A. Goldstein,Joan C. Marini +8 more
TL;DR: Aln treatment improves Brtl femoral geometry and load to fracture but decreases bone matrix synthesis and predicted material modulus and strength, with striking retention of mineralized cartilage.
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Osteogenesis imperfecta: new genes reveal novel mechanisms in bone dysplasia.
TL;DR: The literature is summarized that has contributed to the current understanding of the pathogenesis of OI, a skeletal dysplasia characterized by fragile bones and short stature which is now understood as a collagen-related disorder.
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Rapidly growing Brtl/+ mouse model of osteogenesis imperfecta improves bone mass and strength with sclerostin antibody treatment
Benjamin P. Sinder,Joseph D. Salemi,Michael S. Ominsky,Michelle S. Caird,Joan C. Marini,Kenneth M. Kozloff +5 more
TL;DR: Scl-Ab was able to stimulate bone formation in a rapidly growing Brtl/+ murine model of OI, and represents a potential new therapy to improve bone mass and reduce fracture risk in pediatric OI.