Institution
Saint Francis University
Education•Loretto, Pennsylvania, United States•
About: Saint Francis University is a education organization based out in Loretto, Pennsylvania, United States. It is known for research contribution in the topics: Population & Osteoblast. The organization has 1694 authors who have published 2038 publications receiving 87149 citations.
Topics: Population, Osteoblast, Growth factor, Bone cell, Health care
Papers published on a yearly basis
Papers
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TL;DR: Accumulated data indicate that Dex regulates IGF I and IGF II and their binding proteins differentially in normal human bone marrow stromal cells.
Abstract: Glucocorticoids inhibit the proliferation, but induce the differentiation, of bone marrow stromal cells into osteoblast-like cells. The mechanisms, however, are still conjectural. Since insulin-like growth factors (IGFs) have profound effects on osteoblast growth and differentiation, it is possible that glucocorticoids exert their effects on bone marrow stromal cells in part via regulation of IGFs. Therefore, we analyzed the effects of dexamethasone (Dex) on the expression of IGF I and IGF II in cultured preosteoblastic normal human bone marrow stromal cells (HBMSC). Whereas Dex decreased the concentration of IGF I in the conditioned medium since early in the treatment, the concentration of IGF II was increased progressively as culture period lengthened. As the activities of IGF I and IGF II are regulated by the IGF binding proteins (IGFBPs), we analyzed the effects of Dex on the expression of IGFBPs. Dex increased IGFBP-2 in a time-dependent manner. The increase in IGFBP-2, however, was only to the same extent as that of IGF II at most, depending on the length of treatment. Therefore, the increase in IGFBP-2 would dampen, but not eliminate, the increased IGF II activities. By contrast, Dex decreased IGFBP-3 levels, the latter increasing the bioavailability of IGF II. Although IGFBP-4 mRNA levels were stimulated by Dex, IGFBP-4 concentration in the conditioned medium was unchanged as measured by RIA. IGFBP-5 and IGFBP-6 mRNA levels were decreased by Dex in a time-dependent fashion. IGFBP-5 protein level was also decreased 1–4 days after Dex treatment. IGFBP-1 mRNA was not detectable in HBMSC. These accumulated data indicate that Dex regulates IGF I and IGF II and their binding proteins differentially in normal human bone marrow stromal cells. The progressive increase in IGF II may contribute to Dex-induced cell differentiation. J. Cell. Biochem. 71:449–458, 1998. © 1998 Wiley-Liss, Inc.
60 citations
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TL;DR: An overview of the metabolic response to acute traumatic brain injury is presented, and the feeding methods used to prevent malnutrition and the proper alimentation to diminish the hyperdynamic state and improve immune function are discussed.
Abstract: An overview of the metabolic response to acute traumatic brain injury is presented. The consequences of hypermetabolism, hypercatabolism, and an altered immune function are discussed. Once a person with acute traumatic brain injury develops this hyperdynamic state, the resultant excessive protein breakdown ensues. This can lead to malnutrition. The feeding methods used to prevent malnutrition are discussed, along with the proper alimentation to provide to diminish the hyperdynamic state and improve immune function.
60 citations
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TL;DR: Notch regulates skeletal development and bone remodeling, and gain- or loss-of-function mutations of Notch signaling result in important skeletal diseases.
Abstract: Notch receptors are single-pass transmembrane proteins that determine cell fate. Upon Notch ligand interactions, proteolytic cleavages release the Notch intracellular domain, which translocates to the nucleus to regulate the transcription of target genes, including Hairy enhancer of split (Hes) and Hes related to YRPW motif (Hey). Notch is critical for skeletal development and activity of skeletal cells, and dysregulation of Notch signaling is associated with human diseases affecting the skeleton. Inherited or sporadic mutations in components of the Notch signaling pathway are associated with spondylocostal dysostosis, spondylothoracic dysostosis and recessive brachydactyly, diseases characterized by skeletal patterning defects. Inactivating mutations of the Notch ligand JAG1 or of NOTCH2 are associated with Alagille syndrome, and activating mutations in NOTCH2 are associated with Hajdu-Cheney syndrome (HCS). Individuals affected by HCS exhibit osteolysis in distal phalanges and osteoporosis. NOTCH is activated in selected tumors, such as osteosarcoma, and in breast cancer cells that form osteolytic bone metastases. In conclusion, Notch regulates skeletal development and bone remodeling, and gain- or loss-of-function mutations of Notch signaling result in important skeletal diseases.
60 citations
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TL;DR: Permeability is a critical parameter for understanding subsurface fluid flow behavior, managing reservoirs, enhancing hydrocarbon recovery, and sequestering carbon dioxide as mentioned in this paper, and it is the most common parameter for underground fluid flow.
Abstract: Permeability is a critical parameter for understanding subsurface fluid flow behavior, managing reservoirs, enhancing hydrocarbon recovery, and sequestering carbon dioxide. In general, perm...
59 citations
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TL;DR: DEEP-SDM facilitates content analysis of encounters between women with metastatic breast cancer and their medical oncologists and helps inform the relationship of SDM to patient-reported outcomes.
59 citations
Authors
Showing all 1697 results
Name | H-index | Papers | Citations |
---|---|---|---|
Steven M. Greenberg | 105 | 488 | 44587 |
Linus Pauling | 100 | 536 | 63412 |
Ernesto Canalis | 98 | 331 | 30085 |
John S. Gottdiener | 94 | 316 | 49248 |
Dalane W. Kitzman | 93 | 474 | 36501 |
Joseph F. Polak | 91 | 406 | 38083 |
Charles A. Boucher | 90 | 549 | 31769 |
Lawrence G. Raisz | 82 | 315 | 26147 |
Julius M. Gardin | 76 | 253 | 38063 |
Jeffrey S. Hyams | 72 | 357 | 22166 |
James J. Vredenburgh | 65 | 280 | 18037 |
Michael Centrella | 62 | 120 | 11936 |
Nathaniel Reichek | 62 | 248 | 22847 |
Gerard P. Aurigemma | 59 | 212 | 17127 |
Thomas L. McCarthy | 57 | 107 | 10167 |