PubMed · 137799
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
E M Canalis, G R Mundy, L G Raisz. 1977. Hypercalcemia: diagnosis and therapy.. https://pubmed.ncbi.nlm.nih.gov/137799/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
In 1988, the excellent results obtained with the use of vascularized fibular autograft as a salvage procedure in massive allograft failures caused by non-union or massive resorption prompted a trial of an original reconstructive technique for intercalary defects based on the primary combination of the two types of graft. The authors believe the excellent final results and the ability to avoid further salvage surgical procedures justify the primary application of this more complicated technique despite longer surgical times.
For many years, osteoporosis in women was equated with estrogen deficiency. The recent articles by Zaidi and colleagues offer a new challenge to the estrogen-deficiency-osteoporosis hypothesis by showing that follicle-stimulating hormone (FSH) stimulates osteoclastic bone resorption perhaps through tumor necrosis factor-alpha (TNF-alpha). These authors, however, neglected to mention bone abnormalities and high testosterone levels that were previously shown in FSH-receptor knockout and other modified mice. It is also possible that they have overemphasized potential relationships of these new data with human bone loss. Despite these fascinating data, the paradigm of FSH causing hypogonadal bone loss is not yet ready to displace the estrogen-deficiency-osteoporosis paradigm, although that model already faces considerable challenge.
Human cathepsin K, matrix metalloproteinase 9, and alpha(V)beta(3) integrin are the key regulators in osteoclast-mediated bone resorption. In this paper, we found natural inhibitors 1-10 for them by enzyme inhibition assays. Inhibitors 1-7, 8-9, and 10 are novel inhibitors of human cathepsin K, matrix metalloproteinase 9, and alpha(V)beta(3), respectively.