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The predictive role of symptoms in COVID-19 diagnostic models: A longitudinal insight
- Olivia Bird, Eva P. Galiza, David Neil Baxter, Marta Boffito, Duncan Browne, Fiona Burns, David R. Chadwick, Rebecca Clark, Catherine A. Cosgrove, James Galloway, Anna L. Goodman, Amardeep Heer, Andrew Higham, Shalini Iyengar, Christopher Jeanes, Philip A. Kalra, Christina Kyriakidou, Judy M. Bradley, Chigomezgo Munthali, Angela M. Minassian, Fiona McGill, Patrick Moore, Imrozia Munsoor, Helen Nicholls, Orod Osanlou, Jonathan Packham, Carol H. Pretswell, Alberto San Francisco Ramos, Dinesh Saralaya, Ray P. Sheridan, Richard Smith, Roy L. Soiza, Pauline A. Swift, Emma C. Thomson, Jeremy Turner, Marianne Elizabeth Viljoen, Paul T. Heath, Irina Chis Ster
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- Journal:
- Epidemiology & Infection / Volume 152 / 2024
- Published online by Cambridge University Press:
- 22 January 2024, e37
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To investigate the symptoms of SARS-CoV-2 infection, their dynamics and their discriminatory power for the disease using longitudinally, prospectively collected information reported at the time of their occurrence. We have analysed data from a large phase 3 clinical UK COVID-19 vaccine trial. The alpha variant was the predominant strain. Participants were assessed for SARS-CoV-2 infection via nasal/throat PCR at recruitment, vaccination appointments, and when symptomatic. Statistical techniques were implemented to infer estimates representative of the UK population, accounting for multiple symptomatic episodes associated with one individual. An optimal diagnostic model for SARS-CoV-2 infection was derived. The 4-month prevalence of SARS-CoV-2 was 2.1%; increasing to 19.4% (16.0%–22.7%) in participants reporting loss of appetite and 31.9% (27.1%–36.8%) in those with anosmia/ageusia. The model identified anosmia and/or ageusia, fever, congestion, and cough to be significantly associated with SARS-CoV-2 infection. Symptoms’ dynamics were vastly different in the two groups; after a slow start peaking later and lasting longer in PCR+ participants, whilst exhibiting a consistent decline in PCR- participants, with, on average, fewer than 3 days of symptoms reported. Anosmia/ageusia peaked late in confirmed SARS-CoV-2 infection (day 12), indicating a low discrimination power for early disease diagnosis.
Calcium silicate hydrate (C-S-H) gel dissolution and pH buffering in a cementitious near field
- G. M. N. Baston, A. P. Clacher, T. G. Heath, F. M. I. Hunter, V. Smith, S. W. Swanton
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- Journal:
- Mineralogical Magazine / Volume 76 / Issue 8 / December 2012
- Published online by Cambridge University Press:
- 05 July 2018, pp. 3045-3053
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A cementitious backfill has been proposed in many geological disposal concepts for intermediate-level waste and low-level waste in the UK and elsewhere. In this paper, the main features of the chemical evolution of backfill and the associated changes in the near-field pH are illustrated with results from recent work. For example, interaction of the groundwater with calcium silicate hydrate (C-S-H) phases in a backfill is expected to play an important role in the long-term pH-buffering behaviour. Existing experimental data for the dissolution of C-S-H gels are compared with recent experimental results from leach tests on gels of a lower calcium to silicon ratio (C/S) to provide a consistent set of data across the full C/S range. The results confirm that a congruent dissolution point around C/S = 0.8 is approached by leaching from below (i.e. for gels with 0.29 < C/S < 0.8), as well as from above, as reported elsewhere. In addition, a spreadsheet model has been developed to calculate the volume of backfill required at the vault scale to meet specified pH performance criteria. This model includes the major reactions of the backfill with the groundwater, waste encapsulants and waste components. It can also consider the effects of specific waste packages on local pH performance to allow comparison with the vault-scale calculations.
Genetic and environmental contributions to cannabis dependence in a national young adult twin sample
- M. T. LYNSKEY, A. C. HEATH, E. C. NELSON, K. K. BUCHOLZ, P. A. F. MADDEN, W. S. SLUTSKE, D. J. STATHAM, N. G. MARTIN
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- Journal:
- Psychological Medicine / Volume 32 / Issue 2 / February 2002
- Published online by Cambridge University Press:
- 08 April 2017, pp. 195-207
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Background. This paper examines genetic and environmental contributions to risk of cannabis dependence.
Method. Symptoms of cannabis dependence and measures of social, family and individual risk factors were assessed in a sample of 6265 young adult male and female Australian twins born 1964–1971.
Results. Symptoms of cannabis dependence were common: 11·0% of sample (15·1% of men and 7·8% of women) reported two or more symptoms of dependence. Correlates of cannabis dependence included educational attainment, exposure to parental conflict, sexual abuse, major depression, social anxiety and childhood conduct disorder. However, even after control for the effects of these factors, there was evidence of significant genetic effects on risk of cannabis dependence. Standard genetic modelling indicated that 44·7% (95% CI = 15–72·2) of the variance in liability to cannabis dependence could be accounted for by genetic factors, 20·1% (95% CI = 0–43·6) could be attributed to shared environment factors and 35·3% (95% CI = 26·4–45·7) could be attributed to non-shared environmental factors. However, while there was no evidence of significant gender differences in the magnitude of genetic and environmental influences, a model which assumed both genetic and shared environmental influences on risks of cannabis dependence among men and shared environmental but no genetic influences among women provided an equally good fit to the data.
Conclusions. There was consistent evidence that genetic risk factors are important determinants of risk of cannabis dependence among men. However, it remains uncertain whether there are genetic influences on liability to cannabis dependence among women.
The association between childhood maltreatment, psychopathology, and adult sexual victimization in men and women: results from three independent samples
- K. B. Werner, V. V. McCutcheon, M. Challa, A. Agrawal, M. T. Lynskey, E. Conroy, D. J. Statham, P. A. F. Madden, A. K. Henders, A. A. Todorov, A. C. Heath, L. Degenhardt, N. G. Martin, K. K. Bucholz, E. C. Nelson
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- Journal:
- Psychological Medicine / Volume 46 / Issue 3 / February 2016
- Published online by Cambridge University Press:
- 13 October 2015, pp. 563-573
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Background
Childhood maltreatment (CM) has consistently been linked with adverse outcomes including substance use disorders and adult sexual revictimization. Adult sexual victimization itself has been linked with psychopathology but has predominately been studied in women. The current investigation examines the impact of CM and co-occurring psychopathology on adult sexual victimization in men and women, replicating findings in three distinct samples.
MethodWe investigated the association between continuous CM factor scores and adult sexual victimization in the Childhood Trauma Study (CTS) sample (N = 2564). We also examined the unique relationship between childhood sexual abuse (CSA) and adult sexual victimization while adjusting for co-occurring substance dependence and psychopathology. We replicated these analyses in two additional samples: the Comorbidity and Trauma Study (CATS; N = 1981) and the Australian Twin-Family Study of Alcohol Use Disorders (OZ-ALC; N = 1537).
ResultsAnalyses revealed a significant association with CM factor scores and adult sexual victimization for both men and women across all three samples. The CSA factor score was strongly associated with adult sexual victimization after adjusting for substance dependence and psychopathology; higher odds ratios were observed in men (than women) consistently across the three samples.
ConclusionsA continuous measure of CSA is independently associated with adult sexual trauma risk across samples in models that included commonly associated substance dependence and psychopathology as covariates. The strength of the association between this CSA measure and adult sexual victimization is higher in magnitude for men than women, pointing to the need for further investigation of sexual victimization in male community samples.
The role of conduct disorder in the relationship between alcohol, nicotine and cannabis use disorders
- J. D. Grant, M. T. Lynskey, P. A. F. Madden, E. C. Nelson, L. R. Few, K. K. Bucholz, D. J. Statham, N. G. Martin, A. C. Heath, A. Agrawal
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- Journal:
- Psychological Medicine / Volume 45 / Issue 16 / December 2015
- Published online by Cambridge University Press:
- 18 August 2015, pp. 3505-3515
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Background.
Genetic influences contribute significantly to co-morbidity between conduct disorder and substance use disorders. Estimating the extent of overlap can assist in the development of phenotypes for genomic analyses.
Method.Multivariate quantitative genetic analyses were conducted using data from 9577 individuals, including 3982 complete twin pairs and 1613 individuals whose co-twin was not interviewed (aged 24–37 years) from two Australian twin samples. Analyses examined the genetic correlation between alcohol dependence, nicotine dependence and cannabis abuse/dependence and the extent to which the correlations were attributable to genetic influences shared with conduct disorder.
Results.Additive genetic (a2 = 0.48–0.65) and non-shared environmental factors explained variance in substance use disorders. Familial effects on conduct disorder were due to additive genetic (a2 = 0.39) and shared environmental (c2 = 0.15) factors. All substance use disorders were influenced by shared genetic factors (rg = 0.38–0.56), with all genetic overlap between substances attributable to genetic influences shared with conduct disorder. Genes influencing individual substance use disorders were also significant, explaining 40–73% of the genetic variance per substance.
Conclusions.Among substance users in this sample, the well-documented clinical co-morbidity between conduct disorder and substance use disorders is primarily attributable to shared genetic liability. Interventions targeted at generally reducing deviant behaviors may address the risk posed by this shared genetic liability. However, there is also evidence for genetic and environmental influences specific to each substance. The identification of these substance-specific risk factors (as well as potential protective factors) is critical to the future development of targeted treatment protocols.
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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Contributors
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- By Marcus P. Adams, Robert Bolton, Sanjay Chandrasekharan, Elijah Chudnoff, Edward T. Cokely, William Duggan, Adam Feltz, Roger Giner-Sorolla, Barbara S. Held, Jonathan Jenkins Ichikawa, Chad Kidd, Tara-Marie Linné, Peter Machamer, Farzad Mahootian, Heath Massey, William Meehan, Lisa M. Osbeck, Claude Panaccio, Daniel N. Robinson, Peter Slezak, Thomas Sturm, Paul Thagard
- Edited by Lisa M. Osbeck, University of West Georgia, Barbara S. Held, Bowdoin College, Maine
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- Rational Intuition
- Published online:
- 05 September 2014
- Print publication:
- 25 August 2014, pp vii-viii
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The changing antibiotic susceptibility of bloodstream infections in the first month of life: informing antibiotic policies for early- and late-onset neonatal sepsis
- R. M. BLACKBURN, N. Q. VERLANDER, P. T. HEATH, B. MULLER-PEBODY
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- Journal:
- Epidemiology & Infection / Volume 142 / Issue 4 / April 2014
- Published online by Cambridge University Press:
- 11 July 2013, pp. 803-811
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This study describes the association between antibiotic resistance of bacteria causing neonatal bloodstream infection (BSI) and neonatal age to inform empirical antibiotic treatment guidelines. Antibiotic resistance data were analysed for 14 078 laboratory reports of bacteraemia in neonates aged 0–28 days, received by the Health Protection Agency's (now Public Health England) voluntary surveillance scheme for England and Wales between January 2005 and December 2010. Linear and restricted cubic splines were used in logistic regression models to estimate the nonlinear relationship between age and resistance; the significance of confounding variables was assessed using likelihood ratio tests. An increase in resistance in bacteria causing BSI in neonates aged <4 days was observed, which was greatest between days 2–3 and identified an age (4–8 days, depending on the antibiotic) at which antibiotic resistance plateaus to almost unchanging levels. Our results indicate important age-associated changes in antibiotic resistance and support current empirical treatment guidelines.
Cannabis or alcohol first? Differences by ethnicity and in risk for rapid progression to cannabis-related problems in women
- C. E. Sartor, A. Agrawal, M. T. Lynskey, A. E. Duncan, J. D. Grant, E. C. Nelson, P. A. F. Madden, A. C. Heath, K. K. Bucholz
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- Journal:
- Psychological Medicine / Volume 43 / Issue 4 / April 2013
- Published online by Cambridge University Press:
- 18 July 2012, pp. 813-823
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Background
Initiation of cannabis use typically follows alcohol use, but the reverse order does occur and is more common for African-Americans (AAs) than European-Americans (EAs). The aim of this study was to test for differences in the order of initiation of cannabis and alcohol use between AA and EA women and to determine whether order and ethnicity contribute independently to risk for rapid progression to cannabis-related problems.
MethodData were drawn from structured psychiatric interviews of 4102 women (mean age = 21.6 years), 3787 from an all-female twin study and 315 from a high-risk family study; 18.1% self-identified as AA, 81.9% as EA. Ethnicity and order of initiation of cannabis and alcohol use were modeled as predictors of transition time from first use to onset of cannabis use disorder symptom(s) using Cox proportional hazards regression analyses.
ResultsAA women were nearly three times as likely as EA women to initiate cannabis use before alcohol use. Using cannabis before alcohol [hazard ratio (HR) 1.44, 95% confidence interval (CI) 1.08–1.93] and AA ethnicity (HR 1.59, 95% CI 1.13–2.24) were both associated with rapid progression from first use to cannabis symptom onset even after accounting for age at initiation and psychiatric risk factors.
ConclusionsThe findings indicate that AA women are at greater risk for rapid development of cannabis-related problems than EA women and that this risk is even higher when cannabis use is initiated before alcohol use. Prevention programs should be tailored to the various patterns of cannabis use and relative contributions of risk factors to the development of cannabis-related problems in different ethnic groups.
Do shared etiological factors contribute to the relationship between sexual orientation and depression?
- B. P. Zietsch, K. J. H. Verweij, A. C. Heath, P. A. F. Madden, N. G. Martin, E. C. Nelson, M. T. Lynskey
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- Journal:
- Psychological Medicine / Volume 42 / Issue 3 / March 2012
- Published online by Cambridge University Press:
- 26 August 2011, pp. 521-532
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Background
Gays, lesbians and bisexuals (i.e. non-heterosexuals) have been found to be at much greater risk for many psychiatric symptoms and disorders, including depression. This may be due in part to prejudice and discrimination experienced by non-heterosexuals, but studies controlling for minority stress, or performed in very socially liberal countries, suggest that other mechanisms must also play a role. Here we test the viability of common cause (shared genetic or environmental etiology) explanations of elevated depression rates in non-heterosexuals.
MethodA community-based sample of adult twins (n=9884 individuals) completed surveys investigating the genetics of psychiatric disorder, and were also asked about their sexual orientation. Large subsets of the sample were asked about adverse childhood experiences such as sexual abuse, physical abuse and risky family environment, and also about number of older brothers, paternal and maternal age, and number of close friends. Data were analyzed using the classical twin design.
ResultsNon-heterosexual males and females had higher rates of lifetime depression than their heterosexual counterparts. Genetic factors accounted for 31% and 44% of variation in sexual orientation and depression respectively. Bivariate analysis revealed that genetic factors accounted for a majority (60%) of the correlation between sexual orientation and depression. In addition, childhood sexual abuse and risky family environment were significant predictors of both sexual orientation and depression, further contributing to their correlation.
ConclusionsNon-heterosexual men and women had elevated rates of lifetime depression, partly due to shared etiological factors, although causality cannot be definitively resolved.
Changes in ascertainment of Hib and its influence on the estimation of disease incidence in the United Kingdom
- S. LADHANI, M. P. SLACK, P. T. HEATH, M. E. RAMSAY
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- Journal:
- Epidemiology & Infection / Volume 135 / Issue 5 / July 2007
- Published online by Cambridge University Press:
- 09 November 2006, pp. 861-867
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Enhanced surveillance for Hib infection, initially covering Wales and five English regions, began in 1990 and in 1995 was extended to the whole of England and Wales. To determine whether changes in the ascertainment of Haemophilus influenzae may have affected estimates of Hib disease incidence, data from January 1990 to December 2003 were analysed. A total of 8887 and 4020 (45%) cases of H. influenzae and Hib respectively were reported. The proportion of isolates that were serotyped increased over time, and therefore reported incidence may have underestimated the true incidence in the early years of the study. Adjusting for this under-ascertainment, the incidence in children aged <5 years declined from a peak of 28·3/100 000 in 1991 to 0·97/100 000 in 1998 and increased to 3·8/100 000 in 2003. Following the implementation of universal vaccination a dramatic decline in the true incidence of invasive Hib disease occurred. The observation of the subsequent resurgence was real but the highest incidence reached was 85% below the corrected incidence in the pre-vaccine era. Continued high-quality surveillance is needed in order to accurately monitor and detect changes in disease incidence.
Contrasting models of genetic co-morbidity for cannabis and other illicit drugs in adult Australian twins
- A. AGRAWAL, M. T. LYNSKEY, K. K. BUCHOLZ, N. G. MARTIN, P. A. F. MADDEN, A. C. HEATH
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- Journal:
- Psychological Medicine / Volume 37 / Issue 1 / January 2007
- Published online by Cambridge University Press:
- 01 November 2006, pp. 49-60
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Background. The use of cannabis and other illicit drugs (OIDs) and their co-morbid misuse are frequently reported in the literature. Correlated vulnerabilities and causal or gateway influences have been implicated in this association. We investigated the source of this co-morbidity between cannabis use (experimentation, early and repeated use, and problems) and OID experimentation and problems using genetic models proposed by Neale and Kendler (American Journal of Human Genetics 1995, 57, 935–953).
Method. In a sample of 4152 same-sex male and female adult Australian twin individuals, we fit 13 genetically informative models of co-morbidity to data on experimentation, early use, repeated use of cannabis and co-morbid OID experimentation, and to abuse/dependence (A/D) problems with cannabis and OIDs.
Results. Model-fitting results suggest that common genetic, shared and unique environmental factors are responsible for the association between cannabis experimentation, early use, repeated use and A/D problems and OID experimentation or problems. The liability causation model, which is a reduced form of the correlated vulnerabilities model, also fit very well. In women, we found evidence for high-risk cannabis experimenters and repeated users to be at increased risk for OID experimentation, despite being below the risk threshold on the liability distribution for OID experimentation (extreme multiformity).
Conclusions. Co-morbid cannabis and OID use and misuse are due partly to a common predisposition to substance use disorders. Putative causal effects could not be ruled out. These models warrant further research, so that features of the correlated vulnerabilities model and the gateway models can be studied jointly in a single series of adaptive nested models.
Impact of the Australian Measles Control Campaign on immunity to measles and rubella
- G. L. GILBERT, R. G. ESCOTT, H. F. GIDDING, F. M. TURNBULL, T. C. HEATH, P. B. McINTYRE, M. A. BURGESS
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- Journal:
- Epidemiology & Infection / Volume 127 / Issue 2 / October 2001
- Published online by Cambridge University Press:
- 26 November 2001, pp. 297-303
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To evaluate the impact of the 1998 Australian Measles Control Campaign on immunity to measles and rubella, 4400 opportunistically-collected sera, submitted to diagnostic laboratories across Australia from subjects aged 1–49 years, and 3000 from subjects aged 1–18-years, were tested before and after the campaign, respectively. The proportion of individuals aged 1–18 years who were immune to measles rose from 85% before, to 90% after, the campaign (P < 0·001). The greatest increase was in preschool (7%, P < 0·001) and primary school (10%, P < 0·001) children, who were actively targeted by the campaign. Rubella immunity in 1–18 year-olds rose from 83% to 91% (P < 0·001), again with significant increases in preschool (4%, P = 0·002) and primary school (16%, P < 0·001) children. 94% of individuals aged 19–49 years were immune to rubella. These serosurveys confirm other evidence of the effectiveness of the Australian Measles Control Campaign and demonstrate the value of serosurveillance using opportunistically collected sera.
Childhood sexual abuse and pathogenic parenting in the childhood recollections of adult twin pairs
- T. L. McLAUGHLIN, A. C. HEATH, K. K. BUCHOLZ, P. A. F. MADDEN, L. J. BIERUT, W. S. SLUTSKE, S. DINWIDDIE, D. J. STATHAM, M. P. DUNNE, N. G. MARTIN
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- Journal:
- Psychological Medicine / Volume 30 / Issue 6 / November 2000
- Published online by Cambridge University Press:
- 16 November 2000, pp. 1293-1302
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Background. We examined the relationship between childhood sexual abuse (CSA), and interviewees' recollections of pathogenic parenting, testing for possible retrospective biases in the recollections of those who have experienced CSA.
Methods. Information about CSA, parental divorce and interviewees' recollections of parental rejection, parental overprotection and perceived autonomy (as assessed through a shortened version of the Parental Bonding Instrument) was obtained through telephone interviews with 3626 Australian twins who had also returned self-report questionnaires several years earlier. Recollections of parental behaviours were compared for individuals from pairs in which neither twin, at least one twin, or both twins reported CSA.
Results. Significant associations were noted between CSA and paternal alcoholism and between CSA and recollections of parental rejection. For women, individuals from CSA-discordant pairs reported levels of parental rejection that were significantly higher than those obtained from CSA-negative pairs. The levels of parental rejection observed for twins from CSA-discordant pairs did not differ significantly from those obtained from CSA-concordant pairs, regardless of respondent's abuse status. For men from CSA-discordant pairs, respondents reporting CSA displayed a tendency to report higher levels of parental rejection than did respondents not reporting CSA. Other measures of parenting behaviour (perceived autonomy and parental overprotection) failed to show a clear relationship with CSA.
Conclusions. The relationship between CSA and respondents' recollections of parental rejection is not due solely to retrospective bias on the part of abused individuals and, consistent with other studies, may reflect a pathological family environment with serious consequences for all siblings.
The Hib immunization programme in the Oxford region: an analysis of the impact of vaccine administration on the incidence of disease
- P. G. COEN, P. T. HEATH, G. P. GARNETT
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- Journal:
- Epidemiology & Infection / Volume 123 / Issue 3 / December 1999
- Published online by Cambridge University Press:
- 01 December 1999, pp. 389-402
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In May 1991 an immunization programme against Haemophilus influenzae type b (Hib) infection began within the Oxford region. We validate a deterministic mathematical model of Hib by comparison with the incidence of disease in the Oxford region, 1985–97. The comparison of model results with observed outcome allows an exploration of some of the poorly understood properties of the immunization programme. Model results and observed incidence are consistent with a vaccine that blocks the acquisition of carriage. Similarly, the data suggest that factors other than experience of Hib carriage are likely to have generated acquired immunity to Hib disease prior to the introduction of vaccination. Hence it is unlikely that waning of vaccine-derived protection will result in a resurgence of disease. The inclusion in the immunization schedule of a booster dose, as used in other countries, would have provided very little extra benefit.
The structure of genetic and environmental risk factors for three measures of disordered eating
- T. WADE, N. G. MARTIN, M. C. NEALE, M. TIGGEMANN, S. A. TRELOAR, K. K. BUCHOLZ, P. A. F. MADDEN, A. C. HEATH
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- Journal:
- Psychological Medicine / Volume 29 / Issue 4 / July 1999
- Published online by Cambridge University Press:
- 01 July 1999, pp. 925-934
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Background. The study explored the genetic and environmental risk factors for both the behaviours and attitudes characteristic of disordered eating.
Methods. In three waves of data collection, information was collected from female twins regarding their eating and attitudes towards eating, weight and shape. The first assessment consisted of a self-report questionnaire (1988–9) with 1682 women. The second assessment consisted of a semi-structured psychiatric interview schedule (1992–3), completed by 1852 women, many of whom had completed Wave 1 assessment. The third assessment, with 325 women chosen from Waves 1 and 2 (1995–6), consisted of a semi-structured interview (the Eating Disorder Examination).
Results. As only one twin pair was concordant for lifetime bulimia nervosa at Wave 3 assessment, ordinal measures of all assessments were used in a multivariate genetic analysis. Results indicated that additive genetic and non-shared environmental influences best explained variance in liability to disordered eating, with about 60% (95% CI 50–68) of the variance explained by genetic factors. Comparison with a model allowing for the effects of shared environment indicated genetic factors accounted for a similar degree of variance (59%, 95% CI 36–68).
Conclusion. Liability to the development of the behaviours and attitudes characteristic of eating disorders is best explained by both environmental and genetic factors, with covariation between the three measures best explained by a single latent phenotype of disordered eating which has a heritability of 60%.
Mathematical models of Haemophilus influenzae type b
- P. G. COEN, P. T. HEATH, M. L. BARBOUR, G. P. GARNETT
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- Journal:
- Epidemiology & Infection / Volume 120 / Issue 3 / June 1998
- Published online by Cambridge University Press:
- 01 June 1998, pp. 281-295
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A review of empirical studies and the development of a simple theoretical framework are used to explore the relationship between Haemophilus influenzae type b (Hib) carriage and disease within populations. The models emphasize the distinction between asymptomatic and symptomatic infection. Maximum likelihood methods are used to estimate parameter values of the models and to evaluate whether models of infection and disease are satisfactory. The low incidence of carriage suggests that persistence of infection is only compatible with the absence of acquired immunity to asymptomatic infection. The slight decline in carriage rates amongst adults is compatible with acquired immunity, but could be a consequence of reduced contacts. The low rate of disease observed in adulthood cannot be explained if protection from disease is a product of previous detectable exposure to Hib alone. We estimate an Ro of 3·3 for Hib in developed countries, which suggests that current immunization programmes may eliminate the infection. Analysis of the disease data set suggests the absence of maternal immunity and increased susceptibility to disease in the oldest age classes.
C60 Research at the University of California at Berkeley
- J. R. Heath, J. M. Hawkins, P. A. Alivisatos, R. J. Saykally, T. A. Lewis, S. D. Loren, A. Meyer, Y. Shibato, S. Tolbert, J. Shang
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- Journal:
- MRS Online Proceedings Library Archive / Volume 206 / 1990
- Published online by Cambridge University Press:
- 28 February 2011, 667
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- 1990
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An extremely simple and inexpensive apparatus for preparation of the C60 and C70 fullerenes is described. An efficient separatory technique is described which implements a phenylglycine based HFLC column for preparation of high purity (99.99%) C60 and C70 samples. Treatment of C60 with osmium tetroxide and pyridine gives the osmate ester (2:1 adduct) and establishes that oxygen functionality can be added to C60 without disrupting the carbon framework. Raman spectroscopy of high purity C60 indicates that several lines previously not assigned to C60 (D.S.Bethune, G.Meijer, W.C.Tang, and H.J.Rosen, Chem.Phys.Lett.174, 219(1990)) are attributable to C60.