23 results
5 Antemortem Plasma GFAP Predicts Alzheimer’s Disease Neuropathological Changes
- Madeline Ally, Henrik Zetterberg, Kaj Blennow, Nicholas J. Ashton, Thomas K. Karikari, Hugo Aparicio, Michael A. Sugarman, Brandon Frank, Yorghos Tripodis, Brett Martin, Joseph N. Palmisano, Eric G. Steinberg, Irene Simkina, Lindsay Farrer, Gyungah Jun, Katherine W. Turk, Andrew E. Budson, Maureen K. O’Connor, Rhoda Au, Wei Qiao Qiu, Lee E. Goldstein, Ronald Killiany, Neil W. Kowall, Robert A. Stern, Jesse Mez, Bertran R. Huber, Ann C. McKee, Thor D. Stein, Michael L. Alosco
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- Journal:
- Journal of the International Neuropsychological Society / Volume 29 / Issue s1 / November 2023
- Published online by Cambridge University Press:
- 21 December 2023, pp. 409-410
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Objective:
Blood-based biomarkers offer a more feasible alternative to Alzheimer’s disease (AD) detection, management, and study of disease mechanisms than current in vivo measures. Given their novelty, these plasma biomarkers must be assessed against postmortem neuropathological outcomes for validation. Research has shown utility in plasma markers of the proposed AT(N) framework, however recent studies have stressed the importance of expanding this framework to include other pathways. There is promising data supporting the usefulness of plasma glial fibrillary acidic protein (GFAP) in AD, but GFAP-to-autopsy studies are limited. Here, we tested the association between plasma GFAP and AD-related neuropathological outcomes in participants from the Boston University (BU) Alzheimer’s Disease Research Center (ADRC).
Participants and Methods:This sample included 45 participants from the BU ADRC who had a plasma sample within 5 years of death and donated their brain for neuropathological examination. Most recent plasma samples were analyzed using the Simoa platform. Neuropathological examinations followed the National Alzheimer’s Coordinating Center procedures and diagnostic criteria. The NIA-Reagan Institute criteria were used for the neuropathological diagnosis of AD. Measures of GFAP were log-transformed. Binary logistic regression analyses tested the association between GFAP and autopsy-confirmed AD status, as well as with semi-quantitative ratings of regional atrophy (none/mild versus moderate/severe) using binary logistic regression. Ordinal logistic regression analyses tested the association between plasma GFAP and Braak stage and CERAD neuritic plaque score. Area under the curve (AUC) statistics from receiver operating characteristics (ROC) using predicted probabilities from binary logistic regression examined the ability of plasma GFAP to discriminate autopsy-confirmed AD status. All analyses controlled for sex, age at death, years between last blood draw and death, and APOE e4 status.
Results:Of the 45 brain donors, 29 (64.4%) had autopsy-confirmed AD. The mean (SD) age of the sample at the time of blood draw was 80.76 (8.58) and there were 2.80 (1.16) years between the last blood draw and death. The sample included 20 (44.4%) females, 41 (91.1%) were White, and 20 (44.4%) were APOE e4 carriers. Higher GFAP concentrations were associated with increased odds for having autopsy-confirmed AD (OR=14.12, 95% CI [2.00, 99.88], p=0.008). ROC analysis showed plasma GFAP accurately discriminated those with and without autopsy-confirmed AD on its own (AUC=0.75) and strengthened as the above covariates were added to the model (AUC=0.81). Increases in GFAP levels corresponded to increases in Braak stage (OR=2.39, 95% CI [0.71-4.07], p=0.005), but not CERAD ratings (OR=1.24, 95% CI [0.004, 2.49], p=0.051). Higher GFAP levels were associated with greater temporal lobe atrophy (OR=10.27, 95% CI [1.53,69.15], p=0.017), but this was not observed with any other regions.
Conclusions:The current results show that antemortem plasma GFAP is associated with non-specific AD neuropathological changes at autopsy. Plasma GFAP could be a useful and practical biomarker for assisting in the detection of AD-related changes, as well as for study of disease mechanisms.
24 - Precision Behavioral Management (PBM): A Novel Genetically Guided Therapy to Combat Reward Deficiency Syndrome (RDS) Relevant to the Opiate Crisis
- from Part V - Ongoing and Future Research Directions
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- By Kenneth Blum, Alphonse Kenison Roy, Arwen Podesta, Edward J. Modestino, Bruce Steinberg, Marjorie C. Gondré-Lewis, David Baron, Panayotis K. Thanos, Lisa Lott, Sampada Badgaiyan, Jessica Valdez Ponce, Brent Boyett, David Siwicki, Mark Moran, Drew Edwards, Thomas McLaughlin, Eric R. Braverman, Thomas A. Simpatico, Mary Hauser, Bernard William Downs, Rajendra D. Badgaiyan
- Edited by Steve Sussman, University of Southern California
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- Book:
- The Cambridge Handbook of Substance and Behavioral Addictions
- Published online:
- 13 July 2020
- Print publication:
- 06 August 2020, pp 297-306
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Summary
Reward Deficiency Syndrome (RDS) is an umbrella term for all drug and nondrug addictive behaviors, due to a dopamine deficiency, “hypodopaminergia.” There is an opioid-overdose epidemic in the USA, which may result in or worsen RDS. A paradigm shift is needed to combat a system that is not working. This shift involves the recognition of dopamine homeostasis as the ultimate treatment of RDS via precision, genetically guided KB220 variants, called Precision Behavioral Management (PBM). Recognition of RDS as an endophenotype and an umbrella term in the future DSM 6, following the Research Domain Criteria (RDoC), would assist in shifting this paradigm.
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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A comparison of depression and anxiety symptom trajectories between women who had an abortion and women denied one
- D. G. Foster, J. R. Steinberg, S. C. M. Roberts, J. Neuhaus, M. A. Biggs
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- Journal:
- Psychological Medicine / Volume 45 / Issue 10 / July 2015
- Published online by Cambridge University Press:
- 28 January 2015, pp. 2073-2082
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Background
This study prospectively assesses the mental health outcomes among women seeking abortions, by comparing women having later abortions with women denied abortions, up to 2 years post-abortion seeking.
MethodWe present the first 2 years of a 5-year telephone interview study that is following 956 women who sought an abortion from 30 facilities throughout the USA. We use adjusted linear mixed-effects regression analyses to assess whether symptoms of depression and anxiety, as measured by the Brief Symptom Inventory-short form and the Primary Care Evaluation of Mental Disorders Patient Health Questionnaire, differ over time among women denied an abortion due to advanced gestational age, compared with women who received abortions.
ResultsBaseline predicted mean depressive symptom scores for women denied abortion (3.07) were similar to women receiving an abortion just below the gestational limit (2.86). Depressive symptoms declined over time, with no difference between groups. Initial predicted mean anxiety symptoms were higher among women denied care (2.59) than among women who had an abortion just below the gestational limit (1.91). Anxiety levels in the two groups declined and converged after 1 year.
ConclusionsWomen who received an abortion had similar or lower levels of depression and anxiety than women denied an abortion. Our findings do not support the notion that abortion is a cause of mental health problems.
Contributors
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- By Francesco Acerbi, Ayca Akgoz, Matthew R. Amans, Ramsey Ashour, Mohammed Ali Aziz-Sultan, H. Hunt Batjer, Donnie Bell, Bernard R. Bendok, Giovanni Broggi, Morgan Broggi, Charles A. Bruno, Steven D. Chang, In Sup Choi, Omar Choudhri, Douglas J. Cook, William P. Dillon, Peter Dirks, Rose Du, Travis M. Dumont, Tarek Y. El Ahmadieh, Najib E. El Tecle, Mohamed Samy Elhammady, Paolo Ferroli, Alana M. Flexman, John C. Flickinger, Kai U. Frerichs, Sasikhan Geibprasert, Adrian W. Gelb, Y. Pierre Gobin, Bradley A. Gross, Seunggu J. Han, Tomoki Hashimoto, Juha Hernesniemi, Roberto C. Heros, Steven W. Hetts, Randall T. Higashida, Joshua A. Hirsch, Nikolai J. Hopf, L. Nelson Hopkins, Maziyar A. Kalani, M. Yashar S. Kalani, Hideyuki Kano, Syed Aftab Karim, Robert M. Koffie, Douglas S. Kondziolka, Timo Krings, Aki Laakso, Giuseppe Lanzino, Michael T. Lawton, Elad I. Levy, L. Dade Lunsford, Adel M. Malek, Michael P. Marks, George A. C. Mendes, Philip M. Meyers, Jacques Morcos, Nitin Mukerji, Christian Musahl, Ludmila Pawlikowska, Matthew B. Potts, Ross Puffer, James D. Rabinov, Jonathan J. Russin, Mina G. Safain, Duke Samson, Marco Schiariti, R. Michael Scott, Jason P. Sheehan, Paul Singh, Edward R. Smith, Scott G. Soltys, Robert F. Spetzler, Gary K. Steinberg, Philip E. Stieg, Hua Su, Karel terBrugge, Kiron Thomas, Tarik Tihan, Babu Welch, Jonathan White, H. Richard Winn, Chun-Po Yen, Jacky T. Yeung, Byron Yip, Samer G. Zammar
- Edited by Robert F. Spetzler, Douglas S. Kondziolka, Randall T. Higashida, University of California, San Francisco, M. Yashar S. Kalani
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- Book:
- Comprehensive Management of Arteriovenous Malformations of the Brain and Spine
- Published online:
- 05 January 2015
- Print publication:
- 08 January 2015, pp x-xiv
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Contributors
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- By Lassi Alvesalo, Alberto Anta, Juan Luis Arsuaga, Shara E. Bailey, Priscilla Bayle, José María Bermúdez de Castro, Tracy K. Betsinger, Luca Bondioli, Scott E. Burnett, Concepcion de la Rúa, William N. Duncan, Ryan M. Durner, Heather J.H. Edgar, Scott M. Fitzpatrick, Michael R. Fong, Ana Gracia-Téllez, Theresa M. Grieco, Debbie Guatelli-Steinberg, Tsunehiko Hanihara, Brian E. Hemphill, Leslea J. Hlusko, Michael W. Holmes, Jean-Jacques Hublin, Toby E. Hughes, John P. Hunter, Joel D. Irish, Kent M. Johnson, Sri Kuswandari, Christine Lee, John R. Lukacs, Roberto Macchiarelli, Laura Martín-Francés, Ignacio Martínez, María Martinón-Torres, Arnaud Mazurier, Yuji Mizoguchi, Stephanie Moormann, Greg C. Nelson, Stephen D. Ousley, Oliver T. Rizk, G. Richard Scott, Roman Schomberg, Kes Schroer, Christopher M. Stojanowski, Grant C. Townsend, Christy G. Turner, Theresia C. Weston, Bernard Wood, Clément Zanolli, Linhu Zhang
- Edited by G. Richard Scott, University of Alaska, Fairbanks, Joel D. Irish, Liverpool John Moores University
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- Book:
- Anthropological Perspectives on Tooth Morphology
- Published online:
- 05 March 2013
- Print publication:
- 21 February 2013, pp viii-xi
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Disturbances of basic self and prodromal symptoms among non-psychotic help-seeking adolescents
- D. Koren, N. Reznik, M. Adres, R. Scheyer, A. Apter, T. Steinberg, J. Parnas
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- Journal:
- Psychological Medicine / Volume 43 / Issue 7 / July 2013
- Published online by Cambridge University Press:
- 23 October 2012, pp. 1365-1376
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Background
The goal of this study was to explore the notion that anomalies of self-experience (ASE) are a core, ‘not-yet-psychotic’ clinical phenotype of emerging schizophrenia and its spectrum.
MethodTo accomplish this goal, we examined the relationship between ASE and commonly accepted risk markers in a sample of 87 help-seeking, non-psychotic adolescents (aged 14–18 years). ASE were assessed with the Examination of Anomalous Self-Experience (EASE), subclinical psychotic symptoms were assessed with the Prodromal Questionnaire and the Structured Interview for Prodromal Syndromes, deterioration in psychosocial functioning was assessed with the Social and Role Functioning Scales, and level of distress with the Mood and Anxiety Symptoms Questionnaire.
ResultsAbout 82 participants completed the entire EASE interview. The number of participants who reported ASE at a clinically meaningful level (n = 18, 22%) was smaller than that who met diagnostic criteria for a prodromal syndrome (n = 28, 34%). The degree of overlap between the two conditions was moderate but statistically significant (χ2(1) = 7.01, p = 0.008). An exploratory factor analysis revealed that ASE load on a different factor than prodromal symptoms and deterioration in functioning, but that there is a moderate correlation between the three factors.
ConclusionsThese results suggest that ASE are prevalent among non-psychotic help-seeking adolescents, yet at a considerably lower rate than prodromal symptoms. In addition, they suggest that ASE and prodromal symptoms constitute distinct but moderately related dimensions of potential risk. Taken together, they provide preliminary support for the clinical usefulness of supplementing and refining the methods of early detection of risk with assessment of ASE.
Chapter 18 - Urban Energy Systems
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- By Arnulf Grubler, International Institute for Applied Systems Analysis, Austria and Yale University, Xuemei Bai, Australian National University, Thomas Buettner, United Nations Department of Economic and Social Affairs, Shobhakar Dhakal, Global Carbon Project and National Institute for Environmental Studies, David J. Fisk, Imperial College London, Toshiaki Ichinose, National Institute for Environmental Studies, James E. Keirstead, Imperial College London, Gerd Sammer, University of Natural Resources and Applied Life Sciences, David Satterthwaite, International Institute for Environment and Development, Niels B. Schulz, International Institute for Applied Systems Analysis, Austria and Imperial College, Nilay Shah, Imperial College London, Julia Steinberger, The Institute of Social Ecology, Austria and University of Leeds, Helga Weisz, Potsdam Institute for Climate Impact Research, Gilbert Ahamer, University of Graz, Timothy Baynes, Commonwealth Scientific and Industrial Research Organisation, Daniel Curtis, Oxford University Centre for the Environment, Michael Doherty, Commonwealth Scientific and Industrial Research Organisation, Nick Eyre, Oxford University Centre for the Environment, Junichi Fujino, National Institute for Environmental Studies, Keisuke Hanaki, University of Tokyo, Mikiko Kainuma, National Institute for Environmental Studies, Shinji Kaneko, Hiroshima University, Manfred Lenzen, University of Sydney, Jacqui Meyers, Commonwealth Scientific and Industrial Research Organisation, Hitomi Nakanishi, University of Canberra, Victoria Novikova, Oxford University Centre for the Environment, Krishnan S. Rajan, International Institute of Information Technology, Seongwon Seo, Commonwealth Scientific and Industrial Research Organisation, Ram M. Shrestha, Asian Institute of Technology, Priyadarshi R. Shukla, Indian Institute of Management, Alice Sverdlik, International Institute for Environment and Development, Jayant Sathaye, Lawrence Berkeley National Laboratory
- Global Energy Assessment Writing Team
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- Book:
- Global Energy Assessment
- Published online:
- 05 September 2012
- Print publication:
- 27 August 2012, pp 1307-1400
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Summary
Executive Summary
More than 50% of the global population already lives in urban settlements and urban areas are projected to absorb almost all the global population growth to 2050, amounting to some additional three billion people. Over the next decades the increase in rural population in many developing countries will be overshadowed by population flows to cities. Rural populations globally are expected to peak at a level of 3.5 billion people by around 2020 and decline thereafter, albeit with heterogeneous regional trends. This adds urgency in addressing rural energy access, but our common future will be predominantly urban. Most of urban growth will continue to occur in small-to medium-sized urban centers. Growth in these smaller cities poses serious policy challenges, especially in the developing world. In small cities, data and information to guide policy are largely absent, local resources to tackle development challenges are limited, and governance and institutional capacities are weak, requiring serious efforts in capacity building, novel applications of remote sensing, information, and decision support techniques, and new institutional partnerships. While ‘megacities’ with more than 10 million inhabitants have distinctive challenges, their contribution to global urban growth will remain comparatively small.
Energy-wise, the world is already predominantly urban. This assessment estimates that between 60–80% of final energy use globally is urban, with a central estimate of 75%. Applying national energy (or GHG inventory) reporting formats to the urban scale and to urban administrative boundaries is often referred to as a ‘production’ accounting approach and underlies the above GEA estimate.
Rogues' Gallery of Contributing Authors
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- By Ramon Abola, Rishimani Adsumelli, Syed Azim, Tazeen Beg, Helene Benveniste, Louis Chun, Ramtin Cohanim, Dominick Coleman, Joseph Conrad, Tommy Corrado, Jason Daras, Michelle DiGuglielmo, Vedan Djesevic, Andrew Drollinger, Kathleen Dubrow, Brian Durkin, Ralph Epstein, Christopher J. Gallagher, Xiaojun Guo, Sofie Hussain, Ron Jasiewicz, Anna Kogan, Ursula Landman, Rany Makaryus, Daryn Moller, Tate Montgomery, Matthew Neal, Khoa Nguyen, Marco Palmieri, Shaji Poovathor, Eric Posner, Deborah Richman, Andrew Rozbruch, Misako Sakamaki, Joy Schabel, Bharathi Scott, Peggy Seidman, Shiena Sharma, Vishal Sharma, Ellen Steinberg, Neera Tewari, Jane Yi, Jonida Zeqo, Peter Chung, John Denny, Steven H. Ginsberg, Jeremy Grayson, Jonathan Kraidin, Stephen Lemke, Tejal Patel, Salvatore Zisa, Charles Cowles, Marc Rozner, Shawn Banks, Deborah Brauer, Lebron Cooper, V. Samepathi David, Steve Gayer, Steven Gil, Eric A. Harris, Murlikrishna Kannan, Michael C. Lewis, David A. Lindley, Carlos M. Mijares, Sana Nini, Shafeena Nurani, Sujatha Pentakota, Edgar Pierre, Amy Klash Pulido, Michael Rossi, Miguel Santos, Nancy Setzer-Saade, Adam Sewell, Omair H. Toor, Ashish Udeshi, Patricia Wawroski, Lauren C. Berkow, Dan Berkowitz, Ramola Bhambhani, Kerry K. Blaha, Veronica Busso, Adam J. Carinci, Paul J. Christo, R. Blaine Easley, Ralph J. Fuchs, Samuel M. Galvagno, Nishant Gandhi, Andrew Goins, Robert S. Greenberg, Sayeh Hamzehzadeh, Theresa L. Hartsell, Eugenie Heitmiller, Jeremy M. Huff, Brijen L. Joshi, Sapna Kudchadkar, Jennifer K. Lee, Ira Lehrer, Peter Lin, Justin Lockman, Christine L. Mai, Christina Miller, Nanhi Mitter, Gillian Newman, Daniel Nyhan, Lale Odekon, Rabi Panigrahi, Melissa Pant, Alexander Papangelou, Mark Rossberg, Adam Schiavi, Steven J. Schwartz, Deborah A. Schwengel, Brandon M. Togioka, Tina Tran, Emmett Whitaker, Bradford D. Winters, Christopher Wu, Elena J. Holak, Paul S. Pagel
- Edited by Christopher J. Gallagher, State University of New York, Stony Brook, Michael C. Lewis, University of Miami School of Medicine, Deborah A. Schwengel
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- Book:
- Core Clinical Competencies in Anesthesiology
- Published online:
- 06 July 2010
- Print publication:
- 12 April 2010, pp xi-xii
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Introduction, by David J. Weatherall
- Martin H. Steinberg, Boston University, Bernard G. Forget, Yale University, Connecticut, Douglas R. Higgs, David J. Weatherall, Albert Einstein College of Medicine, New York
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- Disorders of Hemoglobin
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Summary
A few years ago, an eminent British professor of medicine, while reviewing a new edition of a well-known textbook of medicine, suggested that works of this type were becoming valueless because they were already out of date by the time they were published. His derogatory comments went further: Having taken the trouble to weigh the book, he suggested that volumes of this type would suffer the same fate as dinosaurs and become extinct by collapsing under their excessive weight. Even allowing for this bizarre and completely erroneous view of the biological fate of the dinosaurs, does this argument carry any weight beyond its metaphorical context?
Undoubtedly, there is feeling rife among medical publishers that the day of the major monograph in the biological sciences may be coming to an end. They argue that there is so much information online that the need for works of this type is becoming increasingly limited. Is this really the case? Although it is impossible to deny that the long gestation of monographs of this type may lead to the omission of the occasional “breakthrough” in a field, it seems very important that in any rapidly moving area of the biomedical sciences there is a regular and broad critical review of where it has got to and how it has been modified by recent advances. Not uncommonly in medical research and practice, today's breakthrough is tomorrow's breakdown.
Is the hemoglobin field moving rapidly? This was another question that had to be considered by the editors of this new edition.
Index
- Martin H. Steinberg, Boston University, Bernard G. Forget, Yale University, Connecticut, Douglas R. Higgs, David J. Weatherall, Albert Einstein College of Medicine, New York
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- Disorders of Hemoglobin
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Contents
- Martin H. Steinberg, Boston University, Bernard G. Forget, Yale University, Connecticut, Douglas R. Higgs, David J. Weatherall, Albert Einstein College of Medicine, New York
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- Disorders of Hemoglobin
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Preface
- Martin H. Steinberg, Boston University, Bernard G. Forget, Yale University, Connecticut, Douglas R. Higgs, David J. Weatherall, Albert Einstein College of Medicine, New York
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Frontmatter
- Martin H. Steinberg, Boston University, Bernard G. Forget, Yale University, Connecticut, Douglas R. Higgs, David J. Weatherall, Albert Einstein College of Medicine, New York
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- Disorders of Hemoglobin
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List of Contributors
- Martin H. Steinberg, Boston University, Bernard G. Forget, Yale University, Connecticut, Douglas R. Higgs, David J. Weatherall, Albert Einstein College of Medicine, New York
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- Disorders of Hemoglobin
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13 - The Molecular Basis of α Thalassemia
- from SECTION THREE - α THALASSEMIA
- Martin H. Steinberg, Boston University, Bernard G. Forget, Yale University, Connecticut, Douglas R. Higgs, David J. Weatherall, Albert Einstein College of Medicine, New York
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- Disorders of Hemoglobin
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Summary
INTRODUCTION
Before describing the various ways in which α-globin expression may be downregulated in patients with α thalassemia, it is worth briefly reviewing the normal structure of the human α-globin cluster and how the genes are expressed throughout erythroid differentiation and development.
The α-globin cluster is located in a gene dense region of the genome close to the telomere of chromosome 16 (16p13.3). The genes are arranged along the chromosome in the order, telomere-ς-ψς-αD-ψα1-α2-α1-θ-centromere (Fig. 13.1). Upstream of the α cluster there are four highly conserved, noncoding sequences multispecies conserved sequences called MCS-R1–R4 that are thought to be important in the regulation of the α-like globin genes. They correspond to previously identified erythroid-specific DNase l hypersensitive sites (DHS) referred to as HS-48, HS-40, HS-33, and HS-10, the coordinates referring to their positions (kb) with respect to the ς-globin mRNA cap site. Of these elements, only MCS-R2 (HS-40) has been shown to be essential for α globin expression (summarized in Higgs et al.). The role(s) of the other MCS sequences are as yet unclear.
It has been shown that as progenitors commit to the erythroid lineage and differentiate to form mature red cells, a subset of the key erythroid transcription factors and cofactors (Chapter 4) progressively bind the upstream elements and the promoters of the α-like globin genes. Finally, RNA polymerase II is recruited to both the upstream regions and the globin promoters as transcription starts in early and intermediate erythroblasts.
SECTION FOUR - THE β THALASSEMIAS
- Martin H. Steinberg, Boston University, Bernard G. Forget, Yale University, Connecticut, Douglas R. Higgs, David J. Weatherall, Albert Einstein College of Medicine, New York
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Over the years, study of the thalassemia syndromes has served as a paradigm for gaining insights into the factors that can regulate or disrupt normal gene expression. The thalassemias constitute a heterogeneous group of naturally occurring, inherited mutations characterized by abnormal globin gene expression resulting in total absence or quantitative reduction of α- or β-globin chain synthesis in human erythroid cells. α Thalassemia is associated with absent or decreased production of α-chains, whereas in the β thalassemias, there is absent or decreased production of β-chains. In those cases in which some of the affected globin chain is synthesized, early studies demonstrated no evidence of an amino acid substitution. In all cases in which genetic evidence was available, the thalassemia gene appeared to be allelic with the structural gene encoding α- or β-globin. The elucidation of the nature of the various molecular lesions in thalassemia has been a fascinating process, and full of surprises. Increase in our knowledge of the molecular basis of β thalassemia has closely followed and depended on progress and technical breakthroughs in the fields of biochemistry and molecular biology. In particular, recombinant DNA and polymerase chain reaction–based technologies have contributed to a virtual explosion of new information on the precise molecular basis of most forms of thalassemia. The accrual of this knowledge has, to a great degree, paralleled the acquisition of new, detailed information on the structure, organization, and function of the normal human globin genes, as described in the preceding chapters.
SECTION ONE - THE MOLECULAR, CELLULAR, AND GENETIC BASIS OF HEMOGLOBIN DISORDERS
- Martin H. Steinberg, Boston University, Bernard G. Forget, Yale University, Connecticut, Douglas R. Higgs, David J. Weatherall, Albert Einstein College of Medicine, New York
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- Disorders of Hemoglobin
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Over the past 30 years we have become familiar with the way in which different types of hemoglobin are expressed at different stages of development. In the human embryo the main hemoglobins include Hb Portland (ζ2γ2), Hb Gower I (ζ2ε2), and Gower II (α2ε2). In the fetus, HbF (α2γ2) predominates and in the adult, HbA (α2β2) makes up the majority of hemoglobin in red cells. These simple facts belie the complexity of the cellular and molecular processes that bring about these beautifully coordinated changes in the patterns of globin gene expression throughout development.
To understand these phenomena we have to consider the individual components including 1) the origins of erythroid cells in development, 2) the processes by which erythroid cells differentiate to mature red cells at each developmental stage, and 3) the molecular events that produce the patterns of gene expression we observe.
Two different types of erythroid cells are observed during development. The first erythroid cells to be seen in the developing embryo are located in the blood islands of the yolk sac. These primitive erythroid cells are morphologically different from the definitive erythroid cells made in the fetal liver and bone marrow and contain predominantly embryonic hemoglobins. Somewhat later during embryonic development, definitive erythroid and other hematopoietic cells originate from multipotent cells identified in a part of the embryo that lies near the dorsal aorta, in the region close to where the kidneys first develop: the so-called aorta-gonads-mesonephros (AGM) region.
Plate section
- Martin H. Steinberg, Boston University, Bernard G. Forget, Yale University, Connecticut, Douglas R. Higgs, David J. Weatherall, Albert Einstein College of Medicine, New York
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- Disorders of Hemoglobin
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Disorders of Hemoglobin
- Genetics, Pathophysiology, and Clinical Management
- 2nd edition
- Martin H. Steinberg, Bernard G. Forget, Douglas R. Higgs, David J. Weatherall
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- 03 May 2010
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- 17 August 2009
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This book is a completely revised new edition of the definitive reference on disorders of hemoglobin. Authored by world-renowned experts, the book focuses on basic science aspects and clinical features of hemoglobinopathies, covering diagnosis, treatment, and future applications of current research. While the second edition continues to address the important molecular, cellular, and genetic components, coverage of clinical issues has been significantly expanded, and there is more practical emphasis on diagnosis and management throughout. The book opens with a review of the scientific underpinnings. Pathophysiology of common hemoglobin disorders is discussed next in an entirely new section devoted to vascular biology, the erythrocyte membrane, nitric oxide biology, and hemolysis. Four sections deal with α and β thalassemia, sickle cell disease, and related conditions, followed by special topics. The second edition concludes with current and developing approaches to treatment, incorporating new agents for iron chelation, methods to induce fetal hemoglobin production, novel treatment approaches, stem cell transplantation, and progress in gene therapy.