By Health Publica Icon Health Publications
It is a 3-in-1 reference e-book. It provides an entire scientific dictionary protecting 1000s of phrases and expressions in relation to bones. It additionally provides broad lists of bibliographic citations. ultimately, it offers info to clients on tips to replace their wisdom utilizing numerous net assets. The e-book is designed for physicians, scientific scholars getting ready for Board examinations, scientific researchers, and sufferers who are looking to familiarize yourself with study devoted to bones. in the event that your time is effective, this ebook is for you. First, you won't waste time looking out the net whereas lacking loads of proper details. moment, the booklet additionally saves you time indexing and defining entries. ultimately, you won't waste money and time printing 1000s of web content.
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Extra info for Bones - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References
We propose that at least part of the means by which PTH stimulates bone formation is through other growth factors, in particular insulin like growth factor 1 (IGF-1). IGF-1 plays an important role in bone formation, and modulates the ability of PTH to do likewise. The availability of an animal model in which IGF-1 production has been eliminated by homologous recombination provides an opportunity to test the degree to which IGF-1 mediates and/or regulates the skeletal response to PTH. The hypothesis we propose to test is: IGF-1 mediates the anabolic action of PTH on bone by stimulating osteoprogenitor cell proliferation and inhibiting osteoblast apoptosis.
Our long-term goal is to integrate the control of gene expression by Hox transcription factors and metabolic regulation m the proper morphogenesis of craniofacial structures. Knowledge about the interactions of genes with environmental factors will be important for designing therapeutic strategies and preventive measures against craniofacial defects. ; Assistant Professor; Medicine; University of California San Diego 9500 Gilman Dr, Dept. 0934 La Jolla, Ca 92093 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-AUG-2005 Summary: Provided by Applicant): Accumulating evidence has demonstrated that the products of the wnt, frizzled [fzd], secreted frizzled- Irelated protein [SFRP] and LDL receptor-related protein [LRP1 gene families play a critical role in the ]development and maintenance of joints and bones.
The long term objective is to understand the interrelationships among multiple controls, acting through systemic, paracrine, and autocrine mechanisms that are responsible for 38 Bones coordinated long bone growth from embryonic life through adolescence, and to analyze perturbations of growth with the intent of designing and implementing optimal strategies for managing the correction of abnormalities of long bone growth. Using an approach of quantitative measurement of multiple chondrocytic kinetic parameters that completely describe the dynamics of cellular contributions to growth, the Specific Aims of the current proposal are: To test the hypothesis that patterns of differential growth characteristic of specific bones are absent prenatally, but are established starting in the perinatal period and become well defined during early postnatal development, and that this translation is reflected in different cellular control mechanisms; To test the hypothesis that postnatal bone elongation occurs by a pattern of brief intense growth saltations followed by much longer periods of no growth (stasis); To test the hypothesis that the primary action of growth hormone, either circulating systemically or delivered locally, is to increase all rate-dependent phases of chondrocytic differentiation during the postnatal period, thus accelerating rates of differential growth and increasing growth velocity; To test the hypothesis that decreased rate of growth following minimal total nutritional deprivation postnatally, as well as catch-up growth following return to normal nutritional status, are controlled through altering the rate at which chondrocytes at all levels of the growth plate proceed through the differentiation cascade, amplified by volume changes at the level of the hypertrophic chondrocyte.
Bones - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References by Health Publica Icon Health Publications