11 results
TwinsUK: The UK Adult Twin Registry Update
- Serena Verdi, Golboo Abbasian, Ruth C. E. Bowyer, Genevieve Lachance, Darioush Yarand, Paraskevi Christofidou, Massimo Mangino, Cristina Menni, Jordana T. Bell, Mario Falchi, Kerrin S. Small, Frances M. K. Williams, Christopher J. Hammond, Deborah J. Hart, Timothy D. Spector, Claire J. Steves
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- Journal:
- Twin Research and Human Genetics / Volume 22 / Issue 6 / December 2019
- Published online by Cambridge University Press:
- 17 September 2019, pp. 523-529
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TwinsUK is the largest cohort of community-dwelling adult twins in the UK. The registry comprises over 14,000 volunteer twins (14,838 including mixed, single and triplets); it is predominantly female (82%) and middle-aged (mean age 59). In addition, over 1800 parents and siblings of twins are registered volunteers. During the last 27 years, TwinsUK has collected numerous questionnaire responses, physical/cognitive measures and biological measures on over 8500 subjects. Data were collected alongside four comprehensive phenotyping clinical visits to the Department of Twin Research and Genetic Epidemiology, King’s College London. Such collection methods have resulted in very detailed longitudinal clinical, biochemical, behavioral, dietary and socioeconomic cohort characterization; it provides a multidisciplinary platform for the study of complex disease during the adult life course, including the process of healthy aging. The major strength of TwinsUK is the availability of several ‘omic’ technologies for a range of sample types from participants, which includes genomewide scans of single-nucleotide variants, next-generation sequencing, metabolomic profiles, microbiomics, exome sequencing, epigenetic markers, gene expression arrays, RNA sequencing and telomere length measures. TwinsUK facilitates and actively encourages sharing the ‘TwinsUK’ resource with the scientific community — interested researchers may request data via the TwinsUK website (http://twinsuk.ac.uk/resources-for-researchers/access-our-data/) for their own use or future collaboration with the study team. In addition, further cohort data collection is planned via the Wellcome Open Research gateway (https://wellcomeopenresearch.org/gateways). The current article presents an up-to-date report on the application of technological advances, new study procedures in the cohort and future direction of TwinsUK.
The Role of Soil and Landscape Factors in Chinese Privet (Ligustrum sinense) Invasion in the Appalachian Piedmont
- Donald L. Hagan, Elena A. Mikhailova, Timothy M. Shearman, Patrick T. Ma, Jedidah S. Nankaya, Samantha K. Hart, Hillary E. Valdetero, William C. Bridges, He Yun
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- Journal:
- Invasive Plant Science and Management / Volume 7 / Issue 3 / September 2014
- Published online by Cambridge University Press:
- 20 January 2017, pp. 483-490
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There is a limited understanding about the ecological mechanisms that enable certain plant species to become successful invaders of natural areas. This study was conducted to determine the soil and landscape characteristics that correlate with invasion of Chinese privet (CHP), and to develop a model to predict the probability of CHP invasion in Piedmont forests. A landscape ecosystem classification (LEC) system—based on the percentage of clay in the B horizon, depth to maximum clay (cm), exposure, terrain shape, and aspect (degrees)—was used to determine the soil moisture characteristics of invaded and uninvaded plots. Additional measurements included the cover classes of CHP and other species, litter depth (cm), slope (degrees), overstory basal area (m2 ha−1), and soil chemical properties. CHP invasion was negatively correlated with overstory basal area and slope and positively with litter depth and pH. A stepwise logistic regression model containing these four variables was highly sensitive, with an overall accuracy of 78%. Given the accuracy of this model, we propose that it can be used to calculate the probability of invasion in a given area, provided that some basic, readily obtainable site characteristics are known.
Contributors
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- By Mitchell Aboulafia, Frederick Adams, Marilyn McCord Adams, Robert M. Adams, Laird Addis, James W. Allard, David Allison, William P. Alston, Karl Ameriks, C. Anthony Anderson, David Leech Anderson, Lanier Anderson, Roger Ariew, David Armstrong, Denis G. Arnold, E. J. Ashworth, Margaret Atherton, Robin Attfield, Bruce Aune, Edward Wilson Averill, Jody Azzouni, Kent Bach, Andrew Bailey, Lynne Rudder Baker, Thomas R. Baldwin, Jon Barwise, George Bealer, William Bechtel, Lawrence C. Becker, Mark A. Bedau, Ernst Behler, José A. Benardete, Ermanno Bencivenga, Jan Berg, Michael Bergmann, Robert L. Bernasconi, Sven Bernecker, Bernard Berofsky, Rod Bertolet, Charles J. Beyer, Christian Beyer, Joseph Bien, Joseph Bien, Peg Birmingham, Ivan Boh, James Bohman, Daniel Bonevac, Laurence BonJour, William J. Bouwsma, Raymond D. Bradley, Myles Brand, Richard B. Brandt, Michael E. Bratman, Stephen E. Braude, Daniel Breazeale, Angela Breitenbach, Jason Bridges, David O. Brink, Gordon G. Brittan, Justin Broackes, Dan W. Brock, Aaron Bronfman, Jeffrey E. Brower, Bartosz Brozek, Anthony Brueckner, Jeffrey Bub, Lara Buchak, Otavio Bueno, Ann E. Bumpus, Robert W. Burch, John Burgess, Arthur W. Burks, Panayot Butchvarov, Robert E. Butts, Marina Bykova, Patrick Byrne, David Carr, Noël Carroll, Edward S. Casey, Victor Caston, Victor Caston, Albert Casullo, Robert L. Causey, Alan K. L. Chan, Ruth Chang, Deen K. Chatterjee, Andrew Chignell, Roderick M. Chisholm, Kelly J. Clark, E. J. Coffman, Robin Collins, Brian P. Copenhaver, John Corcoran, John Cottingham, Roger Crisp, Frederick J. Crosson, Antonio S. Cua, Phillip D. Cummins, Martin Curd, Adam Cureton, Andrew Cutrofello, Stephen Darwall, Paul Sheldon Davies, Wayne A. Davis, Timothy Joseph Day, Claudio de Almeida, Mario De Caro, Mario De Caro, John Deigh, C. F. Delaney, Daniel C. Dennett, Michael R. DePaul, Michael Detlefsen, Daniel Trent Devereux, Philip E. Devine, John M. Dillon, Martin C. Dillon, Robert DiSalle, Mary Domski, Alan Donagan, Paul Draper, Fred Dretske, Mircea Dumitru, Wilhelm Dupré, Gerald Dworkin, John Earman, Ellery Eells, Catherine Z. Elgin, Berent Enç, Ronald P. Endicott, Edward Erwin, John Etchemendy, C. Stephen Evans, Susan L. Feagin, Solomon Feferman, Richard Feldman, Arthur Fine, Maurice A. Finocchiaro, William FitzPatrick, Richard E. Flathman, Gvozden Flego, Richard Foley, Graeme Forbes, Rainer Forst, Malcolm R. Forster, Daniel Fouke, Patrick Francken, Samuel Freeman, Elizabeth Fricker, Miranda Fricker, Michael Friedman, Michael Fuerstein, Richard A. Fumerton, Alan Gabbey, Pieranna Garavaso, Daniel Garber, Jorge L. A. Garcia, Robert K. Garcia, Don Garrett, Philip Gasper, Gerald Gaus, Berys Gaut, Bernard Gert, Roger F. Gibson, Cody Gilmore, Carl Ginet, Alan H. Goldman, Alvin I. Goldman, Alfonso Gömez-Lobo, Lenn E. Goodman, Robert M. Gordon, Stefan Gosepath, Jorge J. E. Gracia, Daniel W. Graham, George A. Graham, Peter J. Graham, Richard E. Grandy, I. Grattan-Guinness, John Greco, Philip T. Grier, Nicholas Griffin, Nicholas Griffin, David A. Griffiths, Paul J. Griffiths, Stephen R. Grimm, Charles L. Griswold, Charles B. Guignon, Pete A. Y. Gunter, Dimitri Gutas, Gary Gutting, Paul Guyer, Kwame Gyekye, Oscar A. Haac, Raul Hakli, Raul Hakli, Michael Hallett, Edward C. Halper, Jean Hampton, R. James Hankinson, K. R. Hanley, Russell Hardin, Robert M. Harnish, William Harper, David Harrah, Kevin Hart, Ali Hasan, William Hasker, John Haugeland, Roger Hausheer, William Heald, Peter Heath, Richard Heck, John F. Heil, Vincent F. Hendricks, Stephen Hetherington, Francis Heylighen, Kathleen Marie Higgins, Risto Hilpinen, Harold T. Hodes, Joshua Hoffman, Alan Holland, Robert L. Holmes, Richard Holton, Brad W. Hooker, Terence E. Horgan, Tamara Horowitz, Paul Horwich, Vittorio Hösle, Paul Hoβfeld, Daniel Howard-Snyder, Frances Howard-Snyder, Anne Hudson, Deal W. Hudson, Carl A. Huffman, David L. Hull, Patricia Huntington, Thomas Hurka, Paul Hurley, Rosalind Hursthouse, Guillermo Hurtado, Ronald E. Hustwit, Sarah Hutton, Jonathan Jenkins Ichikawa, Harry A. Ide, David Ingram, Philip J. Ivanhoe, Alfred L. Ivry, Frank Jackson, Dale Jacquette, Joseph Jedwab, Richard Jeffrey, David Alan Johnson, Edward Johnson, Mark D. Jordan, Richard Joyce, Hwa Yol Jung, Robert Hillary Kane, Tomis Kapitan, Jacquelyn Ann K. Kegley, James A. Keller, Ralph Kennedy, Sergei Khoruzhii, Jaegwon Kim, Yersu Kim, Nathan L. King, Patricia Kitcher, Peter D. Klein, E. D. Klemke, Virginia Klenk, George L. Kline, Christian Klotz, Simo Knuuttila, Joseph J. Kockelmans, Konstantin Kolenda, Sebastian Tomasz Kołodziejczyk, Isaac Kramnick, Richard Kraut, Fred Kroon, Manfred Kuehn, Steven T. Kuhn, Henry E. Kyburg, John Lachs, Jennifer Lackey, Stephen E. Lahey, Andrea Lavazza, Thomas H. Leahey, Joo Heung Lee, Keith Lehrer, Dorothy Leland, Noah M. Lemos, Ernest LePore, Sarah-Jane Leslie, Isaac Levi, Andrew Levine, Alan E. Lewis, Daniel E. Little, Shu-hsien Liu, Shu-hsien Liu, Alan K. L. Chan, Brian Loar, Lawrence B. Lombard, John Longeway, Dominic McIver Lopes, Michael J. Loux, E. J. Lowe, Steven Luper, Eugene C. Luschei, William G. Lycan, David Lyons, David Macarthur, Danielle Macbeth, Scott MacDonald, Jacob L. Mackey, Louis H. Mackey, Penelope Mackie, Edward H. Madden, Penelope Maddy, G. B. Madison, Bernd Magnus, Pekka Mäkelä, Rudolf A. Makkreel, David Manley, William E. Mann (W.E.M.), Vladimir Marchenkov, Peter Markie, Jean-Pierre Marquis, Ausonio Marras, Mike W. Martin, A. P. Martinich, William L. McBride, David McCabe, Storrs McCall, Hugh J. McCann, Robert N. McCauley, John J. McDermott, Sarah McGrath, Ralph McInerny, Daniel J. McKaughan, Thomas McKay, Michael McKinsey, Brian P. McLaughlin, Ernan McMullin, Anthonie Meijers, Jack W. Meiland, William Jason Melanson, Alfred R. Mele, Joseph R. Mendola, Christopher Menzel, Michael J. Meyer, Christian B. Miller, David W. Miller, Peter Millican, Robert N. Minor, Phillip Mitsis, James A. Montmarquet, Michael S. Moore, Tim Moore, Benjamin Morison, Donald R. Morrison, Stephen J. Morse, Paul K. Moser, Alexander P. D. Mourelatos, Ian Mueller, James Bernard Murphy, Mark C. Murphy, Steven Nadler, Jan Narveson, Alan Nelson, Jerome Neu, Samuel Newlands, Kai Nielsen, Ilkka Niiniluoto, Carlos G. Noreña, Calvin G. Normore, David Fate Norton, Nikolaj Nottelmann, Donald Nute, David S. Oderberg, Steve Odin, Michael O’Rourke, Willard G. Oxtoby, Heinz Paetzold, George S. Pappas, Anthony J. Parel, Lydia Patton, R. P. Peerenboom, Francis Jeffry Pelletier, Adriaan T. Peperzak, Derk Pereboom, Jaroslav Peregrin, Glen Pettigrove, Philip Pettit, Edmund L. Pincoffs, Andrew Pinsent, Robert B. Pippin, Alvin Plantinga, Louis P. Pojman, Richard H. Popkin, John F. Post, Carl J. Posy, William J. Prior, Richard Purtill, Michael Quante, Philip L. Quinn, Philip L. Quinn, Elizabeth S. Radcliffe, Diana Raffman, Gerard Raulet, Stephen L. Read, Andrews Reath, Andrew Reisner, Nicholas Rescher, Henry S. Richardson, Robert C. Richardson, Thomas Ricketts, Wayne D. Riggs, Mark Roberts, Robert C. Roberts, Luke Robinson, Alexander Rosenberg, Gary Rosenkranz, Bernice Glatzer Rosenthal, Adina L. Roskies, William L. Rowe, T. M. Rudavsky, Michael Ruse, Bruce Russell, Lilly-Marlene Russow, Dan Ryder, R. M. Sainsbury, Joseph Salerno, Nathan Salmon, Wesley C. Salmon, Constantine Sandis, David H. Sanford, Marco Santambrogio, David Sapire, Ruth A. Saunders, Geoffrey Sayre-McCord, Charles Sayward, James P. Scanlan, Richard Schacht, Tamar Schapiro, Frederick F. Schmitt, Jerome B. Schneewind, Calvin O. Schrag, Alan D. Schrift, George F. Schumm, Jean-Loup Seban, David N. Sedley, Kenneth Seeskin, Krister Segerberg, Charlene Haddock Seigfried, Dennis M. Senchuk, James F. Sennett, William Lad Sessions, Stewart Shapiro, Tommie Shelby, Donald W. Sherburne, Christopher Shields, Roger A. Shiner, Sydney Shoemaker, Robert K. Shope, Kwong-loi Shun, Wilfried Sieg, A. John Simmons, Robert L. Simon, Marcus G. Singer, Georgette Sinkler, Walter Sinnott-Armstrong, Matti T. Sintonen, Lawrence Sklar, Brian Skyrms, Robert C. Sleigh, Michael Anthony Slote, Hans Sluga, Barry Smith, Michael Smith, Robin Smith, Robert Sokolowski, Robert C. Solomon, Marta Soniewicka, Philip Soper, Ernest Sosa, Nicholas Southwood, Paul Vincent Spade, T. L. S. Sprigge, Eric O. Springsted, George J. Stack, Rebecca Stangl, Jason Stanley, Florian Steinberger, Sören Stenlund, Christopher Stephens, James P. Sterba, Josef Stern, Matthias Steup, M. A. Stewart, Leopold Stubenberg, Edith Dudley Sulla, Frederick Suppe, Jere Paul Surber, David George Sussman, Sigrún Svavarsdóttir, Zeno G. Swijtink, Richard Swinburne, Charles C. Taliaferro, Robert B. Talisse, John Tasioulas, Paul Teller, Larry S. Temkin, Mark Textor, H. S. Thayer, Peter Thielke, Alan Thomas, Amie L. Thomasson, Katherine Thomson-Jones, Joshua C. Thurow, Vzalerie Tiberius, Terrence N. Tice, Paul Tidman, Mark C. Timmons, William Tolhurst, James E. Tomberlin, Rosemarie Tong, Lawrence Torcello, Kelly Trogdon, J. D. Trout, Robert E. Tully, Raimo Tuomela, John Turri, Martin M. Tweedale, Thomas Uebel, Jennifer Uleman, James Van Cleve, Harry van der Linden, Peter van Inwagen, Bryan W. Van Norden, René van Woudenberg, Donald Phillip Verene, Samantha Vice, Thomas Vinci, Donald Wayne Viney, Barbara Von Eckardt, Peter B. M. Vranas, Steven J. Wagner, William J. Wainwright, Paul E. Walker, Robert E. Wall, Craig Walton, Douglas Walton, Eric Watkins, Richard A. Watson, Michael V. Wedin, Rudolph H. Weingartner, Paul Weirich, Paul J. Weithman, Carl Wellman, Howard Wettstein, Samuel C. Wheeler, Stephen A. White, Jennifer Whiting, Edward R. Wierenga, Michael Williams, Fred Wilson, W. Kent Wilson, Kenneth P. Winkler, John F. Wippel, Jan Woleński, Allan B. Wolter, Nicholas P. Wolterstorff, Rega Wood, W. Jay Wood, Paul Woodruff, Alison Wylie, Gideon Yaffe, Takashi Yagisawa, Yutaka Yamamoto, Keith E. Yandell, Xiaomei Yang, Dean Zimmerman, Günter Zoller, Catherine Zuckert, Michael Zuckert, Jack A. Zupko (J.A.Z.)
- Edited by Robert Audi, University of Notre Dame, Indiana
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- The Cambridge Dictionary of Philosophy
- Published online:
- 05 August 2015
- Print publication:
- 27 April 2015, pp ix-xxx
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- By Nazia M. Alam, Enrico Alleva, Hiroyuki Arakawa, Robert H. Benno, Fred G. Biddle, D. Caroline Blanchard, Robert J. Blanchard, Richard J. Bodnar, John D. Boughter, Igor Branchi, Richard E. Brown, Abel Bult-Ito, Jonathan M. Cachat, Peter R. Canavello, Francesca Cirulli, Giovanni Colacicco, John C. Crabbe, Jacqueline N. Crawley, Wim E. Crusio, Sietse F. de Boer, Ekrem Dere, Brenda A. Eales, Robert T. Gerlai, Howard K. Gershenfeld, Thomas J. Gould, Martin E. Hahn, Peter C. Hart, Andrew Holmes, Joseph P. Huston, Allan V. Kalueff, Benjamin Kest, Robert Lalonde, Sarah R. Lewis-Levy, Hans-Peter Lipp, Sheree F. Logue, Stephen C. Maxson, Jeffrey S. Mogil, Douglas A. Monks, Dennis L. Murphy, Lee Niel, Timothy P. O’Leary, Susanna Pietropaolo, Peter K.D. Pilz, Claudia F. Plappert, Bernard Possidente, Glen T. Prusky, Laura Ricceri, Heather Schellinck, Herbert Schwegler, Burton Slotnick, Frans Sluyter, Shad B. Smith, Catherine Strazielle, Douglas Wahlsten, Hans Welzl, James F. Willott, David P. Wolfer, Armin Zlomuzica
- Edited by Wim E. Crusio, Université de Bordeaux, Frans Sluyter, Robert T. Gerlai, University of Toronto, Susanna Pietropaolo, Université de Bordeaux
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- Behavioral Genetics of the Mouse
- Published online:
- 05 May 2013
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- 25 April 2013, pp ix-xii
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Immunolocalization Of Phosphodiesterase Isoenzymes In Rat Tissues Using Confocal Microscopy
- Beverly E. Maleeff, Rosanna C. Mirabile, Timothy K. Hart, Heath C. Thomas, Lester W. Schwartz, Stephen J. Newsholme
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- Journal:
- Microscopy and Microanalysis / Volume 8 / Issue S02 / August 2002
- Published online by Cambridge University Press:
- 01 August 2002, pp. 138-139
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- August 2002
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Microscopic Analysis of Oxidative Stress in Cultured Cells. I. Confocal Microscopy
- Beverly E. Maleeff, Tracy L. Gales, Padma K. Narayanan, Mark A. Tirmenstein, Timothy K. Hart
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- Microscopy and Microanalysis / Volume 7 / Issue S2 / August 2001
- Published online by Cambridge University Press:
- 02 July 2020, pp. 634-635
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- August 2001
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Cellular oxidative stress, a common mechanism of drug-induced toxicity, is a result of the formation of reactive oxygen species (ROS) in response to chemical stimuli. An endpoint of ROS production is lipid peroxidation, which can in turn lead to disruption of cellular membranes, loss of mitochondrial function, protein oxidation and DNA damage. This toxicity can be organ-specific due to the varying capacities of tissues to handle oxidative events. Liver is particularly sensitive to the effects of oxidative stress, and hepatic toxicity is seen clinically. HepG2 cells are an immortalized human hepatoma cell line used as an in vitro model for mammalian hepatotoxicity studies. The purpose of this study was to characterize the effects of chemically induced oxidative stress in this cultured cell model.
HepG2 cells were grown to subconfluence in poly-L-lysine coated 4-well LabTek™ II chambered coverglasses (Nalge Nunc International).
Microscopic Analysis of Oxidative Stress in Cultured Cells. II. Transmission Electron Microscopy
- Tracy L. Gales, Beverly E. Maleeff, Padma K. Narayanan, Mark A. Tirmenstein, Timothy K. Hart
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- Microscopy and Microanalysis / Volume 7 / Issue S2 / August 2001
- Published online by Cambridge University Press:
- 02 July 2020, pp. 636-637
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- August 2001
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The insulin-sensitizing agent troglitazone (Rezulin) has been shown to cause severe hepatotoxicity and liver failure. While the toxic mechanism is still unknown, a component may be oxidative stress. We have demonstrated that increased lipid peroxidation, decreased glutathione levels, and collapse in mitochondrial membrane potential occurred following exposure of cultured hepatocytes to troglitazone. These hallmarks of oxidative stress can manifest morphologically in several ways including damage to cellular membranes, mitochondrial abnormalities, and cell death. The purpose of this study was to assess morphologic changes caused by exposure to troglitazone or cumene hydroperoxide (CH), a compound known to induce oxidative stress.
HepG2 and Novikoff hepatoma cells were grown on poly-L-lysine coated 6-well plates overnight, and exposed to 10, 25, 50 or 100 μM concentrations of troglitazone or CH in the growth media for 2 hours. Cells were fixed with 2.5% glutaraldehyde in phosphate buffer, harvested, and pelleted. Pellets were post-fixed in 1% osmium tetroxide, and processed to epoxy resin.
Nonlinear Dynamics in the Progression of Atherosclerotic Fatty Streaks: Morphometric Analysis
- Peter J. Bugelski, Beverly E. Maleeff, Anne M. Klinkner, Calvert S. Louden, Timothy K. Hart
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- Journal:
- Microscopy and Microanalysis / Volume 6 / Issue 6 / November 2000
- Published online by Cambridge University Press:
- 07 August 2002, pp. 532-541
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- November 2000
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Atherosclerotic lesions are heterogeneous in terms of their cellular and lipid composition. While heterogeneity can be the result of stochastic noise, an alternate hypothesis is that the differences observed among individual lesions arise from deterministic chaos. Five New Zealand white rabbits were fed a diet containing 0.15% cholesterol for 6 months. Segments of the aorta were fixed in formalin, stained en bloc with Nile red (NR) and filipin (F), and en face fluorescence microscopy was used to map the distribution of lipids in fatty streaks (FS). The smallest lesions detected stained only with filipin. Larger lesions stained with both Nile red and filipin and two distinct regions of Nile red staining, NR-orange (rich in polar lipids) and NR-yellow (rich in neutral lipids) were observed. Digital overlays revealed a “nested” arrangement of F, NR-orange, and NR-yellow. The lesions also showed marked heterogeneity in their lipid composition. Thus, although initially similar, as FS increased in size, their composition became divergent, suggesting that the ultimate composition of a FS was highly sensitive to its initial composition. Sensitivity to initial condition is one of the hallmarks of deterministic systems. To determine if FS were self-similar, another hallmark of deterministic chaos, the borders of the different regions defined by NR and F staining were subjected to fractal analysis. For each lesion, the borders of the F, NR-orange, and NR-yellow regions were found to be fractal. Return maps were constructed for the differently stained regions. Analysis of the entire 104-lesion data set showed that although the data could be described by a four-parameter logistic model, the population was not chaotic. However, return maps drawn for the maxima of the NR-orange stained regions demonstrated chaos. Taken together, the data suggest that deterministic chaos plays a role in the evolution of atheromatous disease but, in common with most biologic systems, as the lesions progress, chaotic behavior is dampened.
Clofoctol-Induced Ultrastructural Changes In Staphylococcus Aureus
- Beverly E. Maleeff, Stewart C. Pearson, David J. Payne, Timothy K. Hart
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- Journal:
- Microscopy and Microanalysis / Volume 5 / Issue S2 / August 1999
- Published online by Cambridge University Press:
- 02 July 2020, pp. 1138-1139
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- August 1999
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Clofoctol [2-(2,4-dichlorobenzyl)-4-(tetramethyl-l,l,3,3-butyl) phenol] is a synthetic antibacterial compound with activity against both Gram-positive1 and Gram-negative2 microorganisms. Although the specific mechanism of Clofoctol action has not been fully elucidated, it is reported to alter the permeability of the cytoplasmic membrane in Bacillus subtilis, and is used clinically to treat upper respiratory tract infections in humans. Staphylococcus aureus is a major human Grampositive pathogen that causes a variety of human diseases ranging from localized skin suppuration and food poisoning to life threatening presentations such as septicemia and endocarditis. Several clinical isolates of S. aureus have recently been identified that are resistant to all currently available antibacterial therapies. Consequently, the identification of new antimicrobial targets in this organism is of paramount importance. The purpose of this study was to investigate the in vitro effects of Clofoctol on S. aureus.
Ultrastructural examination of S. aureus revealed a population of actively dividing cells.
Ultrastructural Changes in Hepatocellular Rough Endoplasmic Reticulum in Rats Given a Pyrimidine Derivative
- Beverly E. Maleeff, Stephen J. Newsholme, Timothy K. Hart
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- Journal:
- Microscopy and Microanalysis / Volume 4 / Issue S2 / July 1998
- Published online by Cambridge University Press:
- 02 July 2020, pp. 1060-1061
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- July 1998
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Hepatomegaly, characterized by increased liver weight due to hyperplasia or hypertrophy, can be induced in many species by various drugs or environmental toxins. In rats, hepatomegaly is more usually associated with increases of smooth endoplasmic reticulum in hepatocytes and the associated induction of cytochrome P450 enzymes or with hepatocellular peroxisomal proliferation. In this study, a substituted pyrimidine derivative given to rats resulted in hepatomegaly with an unusual selective increase in hepatocellular rough endoplasmic reticulum (RER).
Female Sprague-Dawley rats were given repeated oral doses of a substituted pyrimidine derivative for 28 consecutive days. Livers were collected at necropsy, weighed, fixed in 10% neutral buffered formalin and processed to paraffin sections stained with hematoxylin and eosin (H&E) for light microscopic evaluation. Portions of formalin-fixed liver were transferred to buffered 2.5% glutaraldehyde for ultrastructural evaluation. Specimens were processed into epoxy resin and thin sections were examined with a JEOL 1200EX transmission electron microscope.
Chemically Induced Accumulation of Phospholipids in Canine Organ Systems. II. Induction by Amiodarone and Chloroquine
- Beverly E. Maleeff, Jeffrey A. Handler, Calvert S. Louden, Timothy K. Hart
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- Journal:
- Microscopy and Microanalysis / Volume 3 / Issue S2 / August 1997
- Published online by Cambridge University Press:
- 02 July 2020, pp. 67-68
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- August 1997
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Cationic amphiphilic drugs (CAD) are structurally characterized by their hydrophobic ring structure and hydrophilic side chain. While there is little known about the effect of CAD in dogs, studies in animal models have shown that over 30 CAD with various pharmacological activities have the ability to induce phospholipid-like inclusions in peripheral blood cells and in organs such as lung, liver, eye and spleen. Two CAD used for treatment of human disease are amiodarone, prescribed for arrythmia, and chloroquine, an antimalarial. The purpose of this study was to determine if these compounds induce cytoplasmic phospholipid inclusions in peripheral blood mononuclear cells (PBMC), polymorphonuclear lymphocytes (PMN), alveloar macrophages, liver and retina in dogs.
Samples were collected from male beagle dogs after 6 weeks of oral dosing with amiodarone (75 mg/kg/day) or chloroquine (75 mg/kg/day). Buffy coats were prepared from peripheral blood and fixed with 3% glutaraldehyde in 0.1 M phosphate buffer, pH 7.2. Alveolar macrophages were recovered from bronchoalveolar lavage fluid by centrifugation and the pellets fixed with buffered 2.5% glutaraldehyde-2% formaldehyde.