985 resultados para Columbia (S.C.)--Canals


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This book gives the history of the South Carolina Chapter 61 of the Telephone Pioneers of America from 1960-2010. These volunteers repair talking book machines for the South Carolina State Library Talking Book Services.

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The consulting firm of Wilbur Smith and Associates was contracted by the South Carolina Department of Archives and History and the city of Columbia through the City's Landmarks Commission to prepare a feasibility study and conceptual master plan for lands adjoining and related to the Columbia Canal. The study area for the project includes the waterfront on both sides of the three Columbia rivers from a mile south of the Blossom Street Bridge on the Congaree to about a half mile south of I-20 on the Broad, and to about a half mile above the Riverbanks Zoo on the Saluda. The recommendations resulting from this study appear in Chapter 10 and are the conclusions of the study team's evaluations summarized i n the nine preceding chapters.

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This proclamation from Governor Mark Sanford proclaims November 2 - 9, 2003 as WIS-TV 50th Anniversary Week.

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TGR5 is a G protein-coupled receptor that mediates bile acid (BA) effects on energy balance, inflammation, digestion and sensation. The mechanisms and spatiotemporal control of TGR5 signaling are poorly understood. We investigated TGR5 signaling and trafficking in transfected HEK293 cells and colonocytes (NCM460) that endogenously express TGR5. BAs (deoxycholic acid, DCA, taurolithocholic acid, TLCA) and the selective agonists oleanolic acid (OA) and 3-(2-chlorophenyl)-N-(4-chlorophenyl)-N, 5-dimethylisoxazole-4-carboxamide (CCDC) stimulated cAMP formation but did not induce TGR5 endocytosis or recruitment of β-arrestins, assessed by confocal microscopy. DCA, TLCA and OA did not stimulate TGR5 association with β-arrestin 1/2 or G protein-coupled receptor kinase (GRK) 2/5/6, determined by bioluminescence resonance energy transfer. CCDC stimulated a low level of TGR5 interaction with β-arrestin2 and GRK2. DCA induced cAMP formation at the plasma membrane and cytosol, determined using exchange factor directly regulated by cAMP (Epac2)-based reporters, but cAMP signals did not desensitize. AG1478, an inhibitor of epidermal growth factor receptor (EGFR) tyrosine kinase, the metalloprotease inhibitor batimastat, and methyl-β-cyclodextrin and filipin, which block lipid raft formation, prevented DCA stimulation of extracellular signal regulated kinase (ERK1/2). BRET analysis revealed TGR5 and EGFR interactions that were blocked by disruption of lipid rafts. DCA stimulated TGR5 redistribution to plasma membrane microdomains, localized by immunogold electron microscopy. Thus, TGR5 does not interact with β-arrestins, desensitize or traffic to endosomes. TGR5 signals from plasma membrane rafts that facilitate EGFR interaction and transactivation. An understanding of the spatiotemporal control of TGR5 signaling provides insights into the actions of BAs and therapeutic TGR5 agonists/antagonists.

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Editors: 1853-Feb. 1867, J.D.B. De Bow -- Apr. 1867-, R.G. Barnwell, E.Q. Bell -- Mar. 1868-Mar. 1869, W.M. Burwell.

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"The fables contained in this volume were ... published in the State between August 1923 and February 1924."

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[v.1] August 25, 1671-June 24, 1680 -- [v.2] April 11, 1692--September 26, 1692.

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Report year irregular.

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National Highway Traffic Safety Administration, Washington, D.C.