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Institution

University of South Carolina

EducationColumbia, South Carolina, United States
About: University of South Carolina is a education organization based out in Columbia, South Carolina, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 25792 authors who have published 59995 publications receiving 2246122 citations. The organization is also known as: USC & U.S.C..


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Journal ArticleDOI
TL;DR: In this paper, a seed-mediated growth approach using ∼4-nm gold nanospheres as the seeds and subsequent reduction of metal salt with a weak reducing agent (ascorbic acid) in the presence of a directing surfactant to produce nanorods.
Abstract: Gold nanorods prepared by a seed-mediated growth approach use ∼4-nm gold nanospheres as the seeds and subsequent reduction of metal salt with a weak reducing agent (ascorbic acid) in the presence of a directing surfactant to produce nanorods. If insufficient ascorbic acid is added in the growth step, then metal salt remains. Additional input of ascorbic acid preferentially deposits more metal at the ends of the nanorods, to yield “dogbone”-like structures. Surprisingly, heat treatment of the unpurified gold nanorods (prepared with an insufficient amount of ascorbic acid) yielded fatter gold nanorods; the oxidation product of ascorbic acid appears to act as a reductant at higher temperature. These modified shapes of the gold nanorods directly influence their optical properties.

482 citations

Journal ArticleDOI
01 May 1994-Diabetes
TL;DR: It is concluded that autoxidation of glucose or Amadori compounds on protein plays a major role in the formation of gly Coxidation products and cross-liking of collagen by glucose in vitro and that chelators, sulfhydryl compounds, antioxidants, and aminoguanidine act as uncouplers of glycation from subsequent glycoxidation andCross-linking reactions.
Abstract: The Maillard or browning reaction between sugar and protein contributes to the increased chemical modification and cross-linking of long-lived tissue proteins in diabetes. To evaluate the role of glycation and oxidation in these reactions, we have studied the effects of oxidative and antioxidative conditions and various types of inhibitors on the reaction of glucose with rat tail tendon collagen in phosphate buffer at physiological pH and temperature. The chemical modifications of collagen that were measured included fructoselysine, the glycoxidation products N epsilon-(carboxymethyl)lysine and pentosidine and fluorescence. Collagen cross-linking was evaluated by analysis of cyanogen bromide peptides using sodium dodecyl sulfate-polyacrylamide gel electrophoresis and by changes in collagen solubilization on treatment with pepsin or sodium dodecylsulfate. Although glycation was unaffected, formation of glycoxidation products and cross-linking of collagen were inhibited by antioxidative conditions. The kinetics of formation of glycoxidation products proceeded with a short lag phase and were independent of the amount of Amadori adduct on the protein, suggesting that autoxidative degradation of glucose was a major contributor to glycoxidation and cross-linking reactions. Chelators, sulfhydryl compounds, antioxidants, and aminoguanidine also inhibited formation of glycoxidation products, generation of fluorescence, and cross-linking of collagen without significant effect on the extent of glycation of the protein. We conclude that autoxidation of glucose or Amadori compounds on protein plays a major role in the formation of glycoxidation products and cross-liking of collagen by glucose in vitro and that chelators, sulfhydryl compounds, antioxidants, and aminoguanidine act as uncouplers of glycation from subsequent glycoxidation and cross-linking reactions.

481 citations

Journal ArticleDOI
09 Feb 2007-Science
TL;DR: Analysis of data from the equatorial Pacific Ocean and Arabian Sea shows that the relative direct and indirect contribution of picoplankton to export is proportional to their total net primary production, despite their small size.
Abstract: Autotrophic picoplankton dominate primary production over large oceanic regions but are believed to contribute relatively little to carbon export from surface layers. Using analyses of data from the equatorial Pacific Ocean and Arabian Sea, we show that the relative direct and indirect contribution of picoplankton to export is proportional to their total net primary production, despite their small size. We suggest that all primary producers, not just the large cells, can contribute to export from the surface layer of the ocean at rates proportional to their production rates.

481 citations

Journal ArticleDOI
TL;DR: In this article, global positioning system data from southern Central America and northwestern South America were collected during 1991, 1994, 1996, and 1998 in Costa Rica, Panama, Ecuador, Colombia, and Venezuela.

480 citations

Journal ArticleDOI
22 Jun 2000-Nature
TL;DR: It is shown that p53 messenger RNA levels are low in a large proportion of breast tumours and loss of expression of p53 in human breast cancer may be primarily due to lack ofexpression of HOXA5.
Abstract: Expression of the p53 gene protects cells against malignant transformation1,2. Whereas control of p53 degradation has been a subject of intense scrutiny, little is known about the factors that regulate p53 synthesis1,2. Here we show that p53 messenger RNA levels are low in a large proportion of breast tumours. Seeking potential regulators of p53 transcription, we found consensus HOX binding sites3,4 in the p53 promoter5. Transient transfection of Hox/HOXA5 activated the p53 promoter. Expression of HOXA5 in epithelial cancer cells expressing wild-type p53, but not in isogenic variants lacking the p53 gene6, led to apoptotic cell death. Moreover, breast cancer cell lines and patient tumours display a coordinate loss of p53 and HOXA5 mRNA and protein expression. The HOXA5 promoter region was methylated in 16 out of 20 p53-negative breast tumour specimens. We conclude that loss of expression of p53 in human breast cancer may be primarily due to lack of expression of HOXA5.

479 citations


Authors

Showing all 26109 results

NameH-indexPapersCitations
Robert M. Califf1961561167961
Eric J. Topol1931373151025
Bernard Rosner1901162147661
Hyun-Chul Kim1764076183227
James F. Sallis169825144836
Steven N. Blair165879132929
Rodney S. Ruoff164666194902
David Cella1561258106402
Claude Bouchard1531076115307
Wei Zheng1511929120209
James M. Tour14385991364
Tim Adye1431898109010
John D. Scott13562583878
Anders Pape Møller135103471713
Lars Klareskog13169763281
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023110
2022503
20213,472
20203,344
20193,000
20182,668