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25 - Modern Literary Production
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- By Martin Rowe
- Edited by Laura Wright, Western Carolina University, North Carolina, Emelia Quinn, Universiteit van Amsterdam
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- Book:
- The Edinburgh Companion to Vegan Literary Studies
- Published by:
- Edinburgh University Press
- Published online:
- 07 June 2023
- Print publication:
- 30 September 2022, pp 349-364
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Summary
Introduction
For thirty years, I was fortunate to be able to pursue twin vocations professionally: book publishing and the cause of animal rights and veganism. This essay provides a personal account of these histories in order to reflect on the specificity of publishing texts that describe and advocate for veganism, and to consider the various market imperatives that have shaped, and continue to shape, the publication, dissemination, and reception of books that espouse veganism. I consider my own experiences forming Lantern Books, a publisher specializing in veganism, animal advocacy, religion, social justice, and psychology, before exploring the role of BISAC codes (the subject categories and subcategories used by bookstores and libraries to catalog books) to provide an example of the limitations the current publishing industry presents for niche publishers – using Sistah Vegan, a book that Lantern published in 2010, as an example. I conclude with reflections from other independent publishers of books on veganism, who speak to the various challenges and rewards of publishing pro-animal books in the current social, politic, and economic publishing climate.
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It was perhaps foreordained that I’d work with books. I read avidly as a child, and studied English Literature and Language at university. My first job was in a bookshop in my hometown in England, which stirred in me a love of the business of writing and selling books. After university, I was hired as a research assistant to the biographer of T. E. Lawrence (of Arabia). I also compiled catalogs for another bookshop and became the mail-order director for a book distributor in London. In 1991, I moved to New York City and completed a master’s degree. During that time, I volunteered at a bookstore, and after graduation I developed marketing material for a publisher. In 1995, Continuum Publishing Company hired me as promotion manager. Four years later, a colleague, Gene Gollogly, and I left to found Lantern.
My second calling was unexpected. I became a vegetarian on something of a whim in 1991 and a vegan when I moved in with my life-partner two years later. In 1994, I co-founded Satya: A Magazine of Vegetarianism, Environmentalism, Animal Advocacy, and Social Justice, a free monthly I edited until I started Lantern. I carried Satya’s subject interests over to Lantern, and over the course of twenty years published over two hundred titles on these subjects.
Aggregation of Abnormal Memory Scores and Risk of Incident Alzheimer’s Disease Dementia: A Measure of Objective Memory Impairment in Amnestic Mild Cognitive Impairment
- Nicholas I. Bradfield, Kathryn A. Ellis, Greg Savage, Paul Maruff, Samantha Burnham, David Darby, Nicola T. Lautenschlager, Ralph N. Martins, Colin L. Masters, Stephanie R. Rainey-Smith, Joanne Robertson, Christopher Rowe, Michael Woodward, David Ames
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- Journal:
- Journal of the International Neuropsychological Society / Volume 27 / Issue 2 / February 2021
- Published online by Cambridge University Press:
- 10 August 2020, pp. 146-157
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Objectives:
The criteria for objective memory impairment in mild cognitive impairment (MCI) are vaguely defined. Aggregating the number of abnormal memory scores (NAMS) is one way to operationalise memory impairment, which we hypothesised would predict progression to Alzheimer’s disease (AD) dementia.
Methods:As part of the Australian Imaging, Biomarkers and Lifestyle Flagship Study of Ageing, 896 older adults who did not have dementia were administered a psychometric battery including three neuropsychological tests of memory, yielding 10 indices of memory. We calculated the number of memory scores corresponding to z ≤ −1.5 (i.e., NAMS) for each participant. Incident diagnosis of AD dementia was established by consensus of an expert panel after 3 years.
Results:Of the 722 (80.6%) participants who were followed up, 54 (7.5%) developed AD dementia. There was a strong correlation between NAMS and probability of developing AD dementia (r = .91, p = .0003). Each abnormal memory score conferred an additional 9.8% risk of progressing to AD dementia. The area under the receiver operating characteristic curve for NAMS was 0.87 [95% confidence interval (CI) .81–.93, p < .01]. The odds ratio for NAMS was 1.67 (95% CI 1.40–2.01, p < .01) after correcting for age, sex, education, estimated intelligence quotient, subjective memory complaint, Mini-Mental State Exam (MMSE) score and apolipoprotein E ϵ4 status.
Conclusions:Aggregation of abnormal memory scores may be a useful way of operationalising objective memory impairment, predicting incident AD dementia and providing prognostic stratification for individuals with MCI.
Alterations in dorsal and ventral posterior cingulate connectivity in APOE ε4 carriers at risk of Alzheimer's disease
- Rebecca Kerestes, Pramit M. Phal, Chris Steward, Bradford A. Moffat, Simon Salinas, Kay L. Cox, Kathryn A. Ellis, Elizabeth V. Cyarto, David Ames, Ralph N. Martins, Colin L. Masters, Christopher C. Rowe, Matthew J. Sharman, Olivier Salvado, Cassandra Szoeke, Michelle Lai, Nicola T. Lautenschlager, Patricia M. Desmond
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- Journal:
- BJPsych Open / Volume 1 / Issue 2 / October 2015
- Published online by Cambridge University Press:
- 02 January 2018, pp. 139-148
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Background
Recent evidence suggests that exercise plays a role in cognition and that the posterior cingulate cortex (PCC) can be divided into dorsal and ventral subregions based on distinct connectivity patterns.
AimsTo examine the effect of physical activity and division of the PCC on brain functional connectivity measures in subjective memory complainers (SMC) carrying the epsilon 4 allele of apolipoprotein E (APOE 4) allele.
MethodParticipants were 22 SMC carrying the APOE ɛ4 allele (ɛ4+; mean age 72.18 years) and 58 SMC non-carriers (ɛ4–; mean age 72.79 years). Connectivity of four dorsal and ventral seeds was examined. Relationships between PCC connectivity and physical activity measures were explored.
Resultsɛ4+ individuals showed increased connectivity between the dorsal PCC and dorsolateral prefrontal cortex, and the ventral PCC and supplementary motor area (SMA). Greater levels of physical activity correlated with the magnitude of ventral PCC–SMA connectivity.
ConclusionsThe results provide the first evidence that ɛ4+ individuals at increased risk of cognitive decline show distinct alterations in dorsal and ventral PCC functional connectivity.
BDNF Val66Met in preclinical Alzheimer's disease is associated with short-term changes in episodic memory and hippocampal volume but not serum mBDNF
- Yen Ying Lim, Stephanie Rainey-Smith, Yoon Lim, Simon M. Laws, Veer Gupta, Tenielle Porter, Pierrick Bourgeat, David Ames, Christopher Fowler, Olivier Salvado, Victor L. Villemagne, Christopher C. Rowe, Colin L. Masters, Xin Fu Zhou, Ralph N. Martins, Paul Maruff
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- Journal:
- International Psychogeriatrics / Volume 29 / Issue 11 / November 2017
- Published online by Cambridge University Press:
- 19 July 2017, pp. 1825-1834
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Background:
The brain-derived neurotrophic factor (BDNF) Val66Met polymorphism Met allele exacerbates amyloid (Aβ) related decline in episodic memory (EM) and hippocampal volume (HV) over 36–54 months in preclinical Alzheimer's disease (AD). However, the extent to which Aβ+ and BDNF Val66Met is related to circulating markers of BDNF (e.g. serum) is unknown. We aimed to determine the effect of Aβ and the BDNF Val66Met polymorphism on levels of serum mBDNF, EM, and HV at baseline and over 18-months.
Methods:Non-demented older adults (n = 446) underwent Aβ neuroimaging and BDNF Val66Met genotyping. EM and HV were assessed at baseline and 18 months later. Fasted blood samples were obtained from each participant at baseline and at 18-month follow-up. Aβ PET neuroimaging was used to classify participants as Aβ– or Aβ+.
Results:At baseline, Aβ+ adults showed worse EM impairment and lower serum mBDNF levels relative to Aβ- adults. BDNF Val66Met polymorphism did not affect serum mBDNF, EM, or HV at baseline. When considered over 18-months, compared to Aβ– Val homozygotes, Aβ+ Val homozygotes showed significant decline in EM and HV but not serum mBDNF. Similarly, compared to Aβ+ Val homozygotes, Aβ+ Met carriers showed significant decline in EM and HV over 18-months but showed no change in serum mBDNF.
Conclusion:While allelic variation in BDNF Val66Met may influence Aβ+ related neurodegeneration and memory loss over the short term, this is not related to serum mBDNF. Longer follow-up intervals may be required to further determine any relationships between serum mBDNF, EM, and HV in preclinical AD.
Comparative analysis of the Cancer Council of Victoria and the online Commonwealth Scientific and Industrial Research Organisation FFQ
- Samantha L. Gardener, Stephanie R. Rainey-Smith, S. Lance Macaulay, Kevin Taddei, Alan Rembach, Paul Maruff, Kathryn A. Ellis, Colin L. Masters, Christopher C. Rowe, David Ames, Jennifer B. Keogh, Ralph N. Martins, The AIBL Research Group
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- Journal:
- British Journal of Nutrition / Volume 114 / Issue 10 / 28 November 2015
- Published online by Cambridge University Press:
- 18 September 2015, pp. 1683-1693
- Print publication:
- 28 November 2015
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FFQ are commonly used to examine the association between diet and disease. They are the most practical method for usual dietary data collection as they are relatively inexpensive and easy to administer. In Australia, the Cancer Council of Victoria FFQ (CCVFFQ) version 2 and the online Commonwealth Scientific and Industrial Research Organisation FFQ (CSIROFFQ) are used. The aim of our study was to establish the level of agreement between nutrient intakes captured using the online CSIROFFQ and the paper-based CCVFFQ. The CCVFFQ and the online CSIROFFQ were completed by 136 healthy participants. FFQ responses were analysed to give g per d intake of a range of nutrients. Agreement between twenty-six nutrient intakes common to both FFQ was measured by a variety of methods. Nutrient intake levels that were significantly correlated between the two FFQ were carbohydrates, total fat, Na and MUFA. When assessing ranking of nutrients into quintiles, on average, 56 % of the participants (for all nutrients) were classified into the same or adjacent quintiles in both FFQ, with the highest percentage agreement for sugar. On average, 21 % of participants were grossly misclassified by three or four quintiles, with the highest percentage misclassification for fibre and Fe. Quintile agreement was similar to that reported by other studies, and we concluded that both FFQ are suitable tools for dividing participants’ nutrient intake levels into high- and low-consumption groups. Use of either FFQ was not appropriate for obtaining accurate estimates of absolute nutrient intakes.
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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- Book:
- The Cambridge Dictionary of Philosophy
- Published online:
- 05 August 2015
- Print publication:
- 27 April 2015, pp ix-xxx
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Autobiographical narratives relate to Alzheimer's disease biomarkers in older adults
- Rachel F. Buckley, Michael M. Saling, Muireann Irish, David Ames, Christopher C. Rowe, Victor L. Villemagne, Nicola T. Lautenschlager, Paul Maruff, S. Lance Macaulay, Ralph N. Martins, Cassandra Szoeke, Colin L. Masters, Stephanie R. Rainey-Smith, Alan Rembach, Greg Savage, Kathryn A. Ellis
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- Journal:
- International Psychogeriatrics / Volume 26 / Issue 10 / October 2014
- Published online by Cambridge University Press:
- 27 June 2014, pp. 1737-1746
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Background:
Autobiographical memory (ABM), personal semantic memory (PSM), and autonoetic consciousness are affected in individuals with mild cognitive impairment (MCI) but their relationship with Alzheimer's disease (AD) biomarkers are unclear.
Methods:Forty-five participants (healthy controls (HC) = 31, MCI = 14) completed the Episodic ABM Interview and a battery of memory tests. Thirty-one (HC = 22, MCI = 9) underwent β-amyloid positron emission tomography (PET) and magnetic resonance (MR) imaging. Fourteen participants (HC = 9, MCI = 5) underwent one imaging modality.
Results:Unlike PSM, ABM differentiated between diagnostic categories but did not relate to AD biomarkers. Personal semantic memory was related to neocortical β-amyloid burden after adjusting for age and apolipoprotein E (APOE) ɛ4. Autonoetic consciousness was not associated with AD biomarkers, and was not impaired in MCI.
Conclusions:Autobiographical memory was impaired in MCI participants but was not related to neocortical amyloid burden, suggesting that personal memory systems are impacted by differing disease mechanisms, rather than being uniformly underpinned by β-amyloid. Episodic and semantic ABM impairment represent an important AD prodrome.
Anxiety symptoms, cerebral amyloid burden and memory decline in healthy older adults without dementia: 3-year prospective cohort study
- Robert H. Pietrzak, J. Cobb Scott, Alexander Neumeister, Yen Ying Lim, David Ames, Kathryn A. Ellis, Karra Harrington, Nicola T. Lautenschlager, Cassandra Szoeke, Ralph N. Martins, Colin L. Masters, Victor L. Villemagne, Christopher C. Rowe, Paul Maruff
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- Journal:
- The British Journal of Psychiatry / Volume 204 / Issue 5 / May 2014
- Published online by Cambridge University Press:
- 02 January 2018, pp. 400-401
- Print publication:
- May 2014
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Although beta-amyloid, anxiety and depression have been linked cross-sectionally to reduced memory function in healthy older adults without dementia, prospective data evaluating these associations are lacking. Using data from an observational cohort study of 178 healthy older adults without dementia followed for 3 years, we found that anxiety symptoms significantly moderated the relationship between beta-amyloid level and decline in verbal (Cohen's d = 0.65) and episodic (Cohen's d = 0.38) memory. Anxiety symptoms were additionally linked to greater decline in executive function, irrespective of beta-amyloid and other risk factors. These findings suggest that interventions to mitigate anxiety symptoms may help delay memory decline in otherwise healthy older adults with elevated beta-amyloid.
Rates of diagnostic transition and cognitive change at 18-month follow-up among 1,112 participants in the Australian Imaging, Biomarkers and Lifestyle Flagship Study of Ageing (AIBL)
- Kathryn A. Ellis, Cassandra Szoeke, Ashley I. Bush, David Darby, Petra L. Graham, Nicola T. Lautenschlager, S. Lance Macaulay, Ralph N. Martins, Paul Maruff, Colin L. Masters, Simon J. McBride, Kerryn E. Pike, Stephanie R. Rainey-Smith, Alan Rembach, Joanne Robertson, Christopher C. Rowe, Greg Savage, Victor L. Villemagne, Michael Woodward, William Wilson, Ping Zhang, David Ames, the AIBL Research Group
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- Journal:
- International Psychogeriatrics / Volume 26 / Issue 4 / April 2014
- Published online by Cambridge University Press:
- 20 November 2013, pp. 543-554
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Background:
The Australian Imaging, Biomarkers and Lifestyle (AIBL) Flagship Study of Ageing is a prospective study of 1,112 individuals (211 with Alzheimer's disease (AD), 133 with mild cognitive impairment (MCI), and 768 healthy controls (HCs)). Here we report diagnostic and cognitive findings at the first (18-month) follow-up of the cohort. The first aim was to compute rates of transition from HC to MCI, and MCI to AD. The second aim was to characterize the cognitive profiles of individuals who transitioned to a more severe disease stage compared with those who did not.
Methods:Eighteen months after baseline, participants underwent comprehensive cognitive testing and diagnostic review, provided an 80 ml blood sample, and completed health and lifestyle questionnaires. A subgroup also underwent amyloid PET and MRI neuroimaging.
Results:The diagnostic status of 89.9% of the cohorts was determined (972 were reassessed, 28 had died, and 112 did not return for reassessment). The 18-month cohort comprised 692 HCs, 82 MCI cases, 197 AD patients, and one Parkinson's disease dementia case. The transition rate from HC to MCI was 2.5%, and cognitive decline in HCs who transitioned to MCI was greatest in memory and naming domains compared to HCs who remained stable. The transition rate from MCI to AD was 30.5%.
Conclusion:There was a high retention rate after 18 months. Rates of transition from healthy aging to MCI, and MCI to AD, were consistent with established estimates. Follow-up of this cohort over longer periods will elucidate robust predictors of future cognitive decline.
The association of Aβ amyloid and composite cognitive measures in healthy older adults and MCI
- Karra D. Harrington, Yen Ying Lim, Kathryn A. Ellis, Carly Copolov, David Darby, Michael Weinborn, David Ames, Ralph N. Martins, Greg Savage, Cassandra Szoeke, Christopher Rowe, Victor L. Villemagne, Colin L. Masters, Paul Maruff
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- Journal:
- International Psychogeriatrics / Volume 25 / Issue 10 / October 2013
- Published online by Cambridge University Press:
- 18 July 2013, pp. 1667-1677
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Background:
To date evidence of the relationship between cognition and Aβ amyloid during the early stages of Alzheimer's Disease (AD) has been inconsistent. This study aimed to describe the nature and magnitude of the relationship between Aβ amyloid and cognitive performance of individuals without dementia.
Methods:Composite cognitive measures were developed from the Australian Imaging Biomarkers and Lifestyle study neuropsychological test battery using data from 768 healthy older adults and 133 adults with mild cognitive impairment (MCI). A subgroup of this sample (174 healthy, 53 MCI) underwent neuroimaging for Aβ amyloid.
Results:Within the MCI group individuals with high Aβ amyloid showed selective impairment for memory compared with those with low Aβ amyloid; however, this difference was not evident in the healthy group.
Conclusions:The current findings provide further evidence of the relationship between Aβ amyloid and cognition, with memory impairment being the primary symptom of the underlying disease during the prodromal phases of AD.
Factors affecting subjective memory complaints in the AIBL aging study: biomarkers, memory, affect, and age
- R. Buckley, M. M. Saling, D. Ames, C. C. Rowe, N. T. Lautenschlager, S. L. Macaulay, R. N. Martins, C. L. Masters, T. O'Meara, G. Savage, C. Szoeke, V. L. Villemagne, K. A. Ellis, Australian Imaging Biomarkers and Lifestyle Study of Aging (AIBL) Research Group
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- Journal:
- International Psychogeriatrics / Volume 25 / Issue 8 / August 2013
- Published online by Cambridge University Press:
- 22 May 2013, pp. 1307-1315
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Background:
The prognostic value of subjective memory complaints (SMCs) in the diagnosis of dementia of the Alzheimer's type is unclear. While some studies have found an association between SMCs and cognitive decline, many have found a stronger association with depression, which raises questions about their diagnostic utility.
Methods:We examined the cross-sectional association between SMC severity (as measured using the MAC-Q, a brief SMC questionnaire) and affect, memory, and Alzheimer's disease (AD) biomarkers (β-amyloid deposition and the apolipoprotein E ε4 (APOEε4) allele) in healthy elderly controls (HC; M = 78.74 years, SD = 6.7) and individuals with mild cognitive impairment (MCI; M = 72.74 years, SD = 8.8). We analyzed a subset of individuals drawn from the Australian Imaging Biomarkers and Lifestyle (AIBL) Study of Aging.
Results:SMCs were more severe in MCI patients than in HCs. SMC severity was related to affective variables and the interaction between age and group membership (HC/MCI). Within the HC group, SMC severity was related to affective variables only, while severity correlated only with age in the MCI group. SMCs were not related to cognitive variables or AD biomarkers.
Conclusion:SMCs were related to solely by poorer mood (greater depressive and anxious symptomatology) in the cognitively healthy elderly however mean levels were subclinical. This finding argues for the assessment of affective symptomatology in conjunction with cognitive assessment in elderly memory complainers. Future AIBL research will focus on assessing other AD biomarkers, such as brain atrophy and Aβ plasma markers, in relation to complaint severity. Once our 36-month follow-up data are collected, we propose to assess whether SMCs can predict future cognitive decline.
Predictors of rapid cognitive decline in Alzheimer's disease: results from the Australian Imaging, Biomarkers and Lifestyle (AIBL) study of ageing
- Alessandro Sona, Ping Zhang, David Ames, Ashley I. Bush, Nicola T. Lautenschlager, Ralph N. Martins, Colin L. Masters, Christopher C. Rowe, Cassandra Szoeke, Kevin Taddei, Kathryn A. Ellis, AIBL Research Group
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- Journal:
- International Psychogeriatrics / Volume 24 / Issue 2 / February 2012
- Published online by Cambridge University Press:
- 13 July 2011, pp. 197-204
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Background: The AIBL study, which commenced in November 2006, is a two-center prospective study of a cohort of 1112 volunteers aged 60+. The cohort includes 211 patients meeting NINCDS-ADRDA criteria for Alzheimer's disease (AD) (180 probable and 31 possible). We aimed to identify factors associated with rapid cognitive decline over 18 months in this cohort of AD patients.
Methods: We defined rapid cognitive decline as a drop of 6 points or more on the Mini-Mental State Examination (MMSE) between baseline and 18-month follow-up. Analyses were also conducted with a threshold of 4, 5, 7 and 8 points, as well as with and without subjects who had died or were too severely affected to be interviewed at 18 months and after, both including and excluding subjects whose AD diagnosis was “possible” AD. We sought correlations between rapid cognitive decline and demographic, clinical and biological variables.
Results: Of the 211 AD patients recruited at baseline, we had available data for 156 (73.9%) patients at 18 months. Fifty-one patients were considered rapid cognitive decliners (32.7%). A higher Clinical Dementia Rating scale (CDR) and higher CDR “sum of boxes” score at baseline were the major predictors of rapid cognitive decline in this population. Furthermore, using logistic regression model analysis, patients treated with a cholinesterase inhibitor (CheI) had a higher risk of being rapid cognitive decliners, as did males and those of younger age.
Conclusions: Almost one third of patients satisfying established research criteria for AD experienced rapid cognitive decline. Worse baseline functional and cognitive status and treatment with a CheI were the major factors associated with rapid cognitive decline over 18 months in this population.
Tight Bounds for Blind Search on the Integers and the Reals
- MARTIN DIETZFELBINGER, JONATHAN E. ROWE, INGO WEGENER, PHILIPP WOELFEL
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- Journal:
- Combinatorics, Probability and Computing / Volume 19 / Issue 5-6 / November 2010
- Published online by Cambridge University Press:
- 18 December 2009, pp. 711-728
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We analyse a simple random process in which a token is moved in the interval A = {0, . . ., n}. Fix a probability distribution μ over D = {1, . . ., n}. Initially, the token is placed in a random position in A. In round t, a random step sized is chosen according to μ. If the token is in position x ≥ d, then it is moved to position x − d. Otherwise it stays put. Let TX be the number of rounds until the token reaches position 0. We show tight bounds for the expectation Eμ(TX) of TX for varying distributions μ. More precisely, we show that . The same bounds are proved for the analogous continuous process, where step sizes and token positions are real values in [0, n + 1), and one measures the time until the token has reached a point in [0, 1). For the proofs, a novel potential function argument is introduced. The research is motivated by the problem of approximating the minimum of a continuous function over [0, 1] with a ‘blind’ optimization strategy.
The Australian Imaging, Biomarkers and Lifestyle (AIBL) study of aging: methodology and baseline characteristics of 1112 individuals recruited for a longitudinal study of Alzheimer's disease
- Kathryn A Ellis, Ashley I Bush, David Darby, Daniela De Fazio, Jonathan Foster, Peter Hudson, Nicola T. Lautenschlager, Nat Lenzo, Ralph N. Martins, Paul Maruff, Colin Masters, Andrew Milner, Kerryn Pike, Christopher Rowe, Greg Savage, Cassandra Szoeke, Kevin Taddei, Victor Villemagne, Michael Woodward, David Ames, the AIBL Research Group
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- Journal:
- International Psychogeriatrics / Volume 21 / Issue 4 / August 2009
- Published online by Cambridge University Press:
- 01 August 2009, pp. 672-687
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Background: The Australian Imaging, Biomarkers and Lifestyle (AIBL) flagship study of aging aimed to recruit 1000 individuals aged over 60 to assist with prospective research into Alzheimer's disease (AD). This paper describes the recruitment of the cohort and gives information about the study methodology, baseline demography, diagnoses, medical comorbidities, medication use, and cognitive function of the participants.
Methods: Volunteers underwent a screening interview, had comprehensive cognitive testing, gave 80 ml of blood, and completed health and lifestyle questionnaires. One quarter of the sample also underwent amyloid PET brain imaging with Pittsburgh compound B (PiB PET) and MRI brain imaging, and a subgroup of 10% had ActiGraph activity monitoring and body composition scanning.
Results: A total of 1166 volunteers were recruited, 54 of whom were excluded from further study due to comorbid disorders which could affect cognition or because of withdrawal of consent. Participants with AD (211) had neuropsychological profiles which were consistent with AD, and were more impaired than participants with mild cognitive impairment (133) or healthy controls (768), who performed within expected norms for age on neuropsychological testing. PiB PET scans were performed on 287 participants, 100 had DEXA scans and 91 participated in ActiGraph monitoring.
Conclusion: The participants comprising the AIBL cohort represent a group of highly motivated and well-characterized individuals who represent a unique resource for the study of AD. They will be reassessed at 18-month intervals in order to determine the predictive utility of various biomarkers, cognitive parameters and lifestyle factors as indicators of AD, and as predictors of future cognitive decline.
11 - Cellular adhesion molecules and MHC antigens in cells infected with Epstein-Barr virus: implications for immune recognition
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- By Martin Rowe, University of Birmingham, Maria G. Masucci, Karolinska Institute
- Edited by G. Eric Blair, University of Leeds, Craig R. Pringle, University of Warwick, D. John Maudsley, University of Warwick
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- Book:
- Modulation of MHC Antigen Expression and Disease
- Published online:
- 11 September 2009
- Print publication:
- 09 November 1995, pp 261-277
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Summary
Introduction: the CTL response to Epstein–Barr virus
Epstein–Barr virus (EBV) is a γ-herpesvirus that is carried by more than 90% of adults worldwide as an asymptomatic persistent infection. This virus is the causative agent of infectious mononucleosis, a benign lymphoproliferative disease and is also implicated in the pathogenesis of an increasing number of malignant diseases, including: Burkitt's lymphoma (BL), nasopharyngeal carcinoma and Hodgkin's disease (Miller, 1990). The importance of cellular immunity, and especially of CTLs, in controlling the potentially harmful consequences of EBV infection is underscored by the increased incidence of EBV-driven lymphoproliferations in organ transplant recipients receiving immunosuppressive therapy and in AIDS patients (Thomas, Allday & Crawford, 1991).
The pathogenic potential of EBV is well illustrated by the ease with which the virus can infect resting B lymphocytes in vitro, causing growth-transformation and the establishment of lymphoblastoid cell lines (LCLs) with infinite doubling capacity. This in vitro infection model provided the first clue as to how the virus is controlled in vivo. If circulating lymphocytes from EBV-seropositive donors are infected with EBV in vitro without first removing or inactivating the T lymphocytes, then the initial proliferation of EBV-infected B lymphocytes is followed by a regression at two to three weeks post-infection because of reactivation of EBV-specific memory T lymphocytes that eliminate the virus-infected cells (Rickinson et al, 1981). Activated T cells isolated from such cultures contain CTL populations that are HLA class I-restricted and specific for EBV-encoded antigens.