17 results
Characterisation of age and polarity at onset in bipolar disorder
- Janos L. Kalman, Loes M. Olde Loohuis, Annabel Vreeker, Andrew McQuillin, Eli A. Stahl, Douglas Ruderfer, Maria Grigoroiu-Serbanescu, Georgia Panagiotaropoulou, Stephan Ripke, Tim B. Bigdeli, Frederike Stein, Tina Meller, Susanne Meinert, Helena Pelin, Fabian Streit, Sergi Papiol, Mark J. Adams, Rolf Adolfsson, Kristina Adorjan, Ingrid Agartz, Sofie R. Aminoff, Heike Anderson-Schmidt, Ole A. Andreassen, Raffaella Ardau, Jean-Michel Aubry, Ceylan Balaban, Nicholas Bass, Bernhard T. Baune, Frank Bellivier, Antoni Benabarre, Susanne Bengesser, Wade H Berrettini, Marco P. Boks, Evelyn J. Bromet, Katharina Brosch, Monika Budde, William Byerley, Pablo Cervantes, Catina Chillotti, Sven Cichon, Scott R. Clark, Ashley L. Comes, Aiden Corvin, William Coryell, Nick Craddock, David W. Craig, Paul E. Croarkin, Cristiana Cruceanu, Piotr M. Czerski, Nina Dalkner, Udo Dannlowski, Franziska Degenhardt, Maria Del Zompo, J. Raymond DePaulo, Srdjan Djurovic, Howard J. Edenberg, Mariam Al Eissa, Torbjørn Elvsåshagen, Bruno Etain, Ayman H. Fanous, Frederike Fellendorf, Alessia Fiorentino, Andreas J. Forstner, Mark A. Frye, Janice M. Fullerton, Katrin Gade, Julie Garnham, Elliot Gershon, Michael Gill, Fernando S. Goes, Katherine Gordon-Smith, Paul Grof, Jose Guzman-Parra, Tim Hahn, Roland Hasler, Maria Heilbronner, Urs Heilbronner, Stephane Jamain, Esther Jimenez, Ian Jones, Lisa Jones, Lina Jonsson, Rene S. Kahn, John R. Kelsoe, James L. Kennedy, Tilo Kircher, George Kirov, Sarah Kittel-Schneider, Farah Klöhn-Saghatolislam, James A. Knowles, Thorsten M. Kranz, Trine Vik Lagerberg, Mikael Landen, William B. Lawson, Marion Leboyer, Qingqin S. Li, Mario Maj, Dolores Malaspina, Mirko Manchia, Fermin Mayoral, Susan L. McElroy, Melvin G. McInnis, Andrew M. McIntosh, Helena Medeiros, Ingrid Melle, Vihra Milanova, Philip B. Mitchell, Palmiero Monteleone, Alessio Maria Monteleone, Markus M. Nöthen, Tomas Novak, John I. Nurnberger, Niamh O'Brien, Kevin S. O'Connell, Claire O'Donovan, Michael C. O'Donovan, Nils Opel, Abigail Ortiz, Michael J. Owen, Erik Pålsson, Carlos Pato, Michele T. Pato, Joanna Pawlak, Julia-Katharina Pfarr, Claudia Pisanu, James B. Potash, Mark H Rapaport, Daniela Reich-Erkelenz, Andreas Reif, Eva Reininghaus, Jonathan Repple, Hélène Richard-Lepouriel, Marcella Rietschel, Kai Ringwald, Gloria Roberts, Guy Rouleau, Sabrina Schaupp, William A Scheftner, Simon Schmitt, Peter R. Schofield, K. Oliver Schubert, Eva C. Schulte, Barbara Schweizer, Fanny Senner, Giovanni Severino, Sally Sharp, Claire Slaney, Olav B. Smeland, Janet L. Sobell, Alessio Squassina, Pavla Stopkova, John Strauss, Alfonso Tortorella, Gustavo Turecki, Joanna Twarowska-Hauser, Marin Veldic, Eduard Vieta, John B. Vincent, Wei Xu, Clement C. Zai, Peter P. Zandi, Psychiatric Genomics Consortium (PGC) Bipolar Disorder Working Group, International Consortium on Lithium Genetics (ConLiGen), Colombia-US Cross Disorder Collaboration in Psychiatric Genetics, Arianna Di Florio, Jordan W. Smoller, Joanna M. Biernacka, Francis J. McMahon, Martin Alda, Bertram Müller-Myhsok, Nikolaos Koutsouleris, Peter Falkai, Nelson B. Freimer, Till F.M. Andlauer, Thomas G. Schulze, Roel A. Ophoff
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- Journal:
- The British Journal of Psychiatry / Volume 219 / Issue 6 / December 2021
- Published online by Cambridge University Press:
- 25 August 2021, pp. 659-669
- Print publication:
- December 2021
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Background
Studying phenotypic and genetic characteristics of age at onset (AAO) and polarity at onset (PAO) in bipolar disorder can provide new insights into disease pathology and facilitate the development of screening tools.
AimsTo examine the genetic architecture of AAO and PAO and their association with bipolar disorder disease characteristics.
MethodGenome-wide association studies (GWASs) and polygenic score (PGS) analyses of AAO (n = 12 977) and PAO (n = 6773) were conducted in patients with bipolar disorder from 34 cohorts and a replication sample (n = 2237). The association of onset with disease characteristics was investigated in two of these cohorts.
ResultsEarlier AAO was associated with a higher probability of psychotic symptoms, suicidality, lower educational attainment, not living together and fewer episodes. Depressive onset correlated with suicidality and manic onset correlated with delusions and manic episodes. Systematic differences in AAO between cohorts and continents of origin were observed. This was also reflected in single-nucleotide variant-based heritability estimates, with higher heritabilities for stricter onset definitions. Increased PGS for autism spectrum disorder (β = −0.34 years, s.e. = 0.08), major depression (β = −0.34 years, s.e. = 0.08), schizophrenia (β = −0.39 years, s.e. = 0.08), and educational attainment (β = −0.31 years, s.e. = 0.08) were associated with an earlier AAO. The AAO GWAS identified one significant locus, but this finding did not replicate. Neither GWAS nor PGS analyses yielded significant associations with PAO.
ConclusionsAAO and PAO are associated with indicators of bipolar disorder severity. Individuals with an earlier onset show an increased polygenic liability for a broad spectrum of psychiatric traits. Systematic differences in AAO across cohorts, continents and phenotype definitions introduce significant heterogeneity, affecting analyses.
Impact of schizophrenia genetic liability on the association between schizophrenia and physical illness: data-linkage study
- Kimberley M. Kendall, Ann John, Sze Chim Lee, Elliott Rees, Antonio F. Pardiñas, Marcos Del Pozo Banos, Michael J. Owen, Michael C. O'Donovan, George Kirov, Keith Lloyd, Ian Jones, Sophie E. Legge, James T. R. Walters
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- Journal:
- BJPsych Open / Volume 6 / Issue 6 / November 2020
- Published online by Cambridge University Press:
- 10 November 2020, e139
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Background
Individuals with schizophrenia are at higher risk of physical illnesses, which are a major contributor to their 20-year reduced life expectancy. It is currently unknown what causes the increased risk of physical illness in schizophrenia.
AimsTo link genetic data from a clinically ascertained sample of individuals with schizophrenia to anonymised National Health Service (NHS) records. To assess (a) rates of physical illness in those with schizophrenia, and (b) whether physical illness in schizophrenia is associated with genetic liability.
MethodWe linked genetic data from a clinically ascertained sample of individuals with schizophrenia (Cardiff Cognition in Schizophrenia participants, n = 896) to anonymised NHS records held in the Secure Anonymised Information Linkage (SAIL) databank. Physical illnesses were defined from the General Practice Database and Patient Episode Database for Wales. Genetic liability for schizophrenia was indexed by (a) rare copy number variants (CNVs), and (b) polygenic risk scores.
ResultsIndividuals with schizophrenia in SAIL had increased rates of epilepsy (standardised rate ratio (SRR) = 5.34), intellectual disability (SRR = 3.11), type 2 diabetes (SRR = 2.45), congenital disorders (SRR = 1.77), ischaemic heart disease (SRR = 1.57) and smoking (SRR = 1.44) in comparison with the general SAIL population. In those with schizophrenia, carrier status for schizophrenia-associated CNVs and neurodevelopmental disorder-associated CNVs was associated with height (P = 0.015–0.017), with carriers being 7.5–7.7 cm shorter than non-carriers. We did not find evidence that the increased rates of poor physical health outcomes in schizophrenia were associated with genetic liability for the disorder.
ConclusionsThis study demonstrates the value of and potential for linking genetic data from clinically ascertained research studies to anonymised health records. The increased risk for physical illness in schizophrenia is not caused by genetic liability for the disorder.
Examining pathways between genetic liability for schizophrenia and patterns of tobacco and cannabis use in adolescence
- Hannah J. Jones, Gemma Hammerton, Tayla McCloud, Lindsey A. Hines, Caroline Wright, Suzanne H. Gage, Peter Holmans, Peter B Jones, George Davey Smith, David E. J. Linden, Michael C. O'Donovan, Michael J. Owen, James T. Walters, Marcus R. Munafò, Jon Heron, Stanley Zammit
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- Journal:
- Psychological Medicine / Volume 52 / Issue 1 / January 2022
- Published online by Cambridge University Press:
- 09 June 2020, pp. 132-139
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Background
It is not clear to what extent associations between schizophrenia, cannabis use and cigarette use are due to a shared genetic etiology. We, therefore, examined whether schizophrenia genetic risk associates with longitudinal patterns of cigarette and cannabis use in adolescence and mediating pathways for any association to inform potential reduction strategies.
MethodsAssociations between schizophrenia polygenic scores and longitudinal latent classes of cigarette and cannabis use from ages 14 to 19 years were investigated in up to 3925 individuals in the Avon Longitudinal Study of Parents and Children. Mediation models were estimated to assess the potential mediating effects of a range of cognitive, emotional, and behavioral phenotypes.
ResultsThe schizophrenia polygenic score, based on single nucleotide polymorphisms meeting a training-set p threshold of 0.05, was associated with late-onset cannabis use (OR = 1.23; 95% CI = 1.08,1.41), but not with cigarette or early-onset cannabis use classes. This association was not mediated through lower IQ, victimization, emotional difficulties, antisocial behavior, impulsivity, or poorer social relationships during childhood. Sensitivity analyses adjusting for genetic liability to cannabis or cigarette use, using polygenic scores excluding the CHRNA5-A3-B4 gene cluster, or basing scores on a 0.5 training-set p threshold, provided results consistent with our main analyses.
ConclusionsOur study provides evidence that genetic risk for schizophrenia is associated with patterns of cannabis use during adolescence. Investigation of pathways other than the cognitive, emotional, and behavioral phenotypes examined here is required to identify modifiable targets to reduce the public health burden of cannabis use in the population.
Clinical indicators of treatment-resistant psychosis
- Sophie E. Legge, Charlotte A. Dennison, Antonio F. Pardiñas, Elliott Rees, Amy J. Lynham, Lucinda Hopkins, Lesley Bates, George Kirov, Michael J. Owen, Michael C. O'Donovan, James T.R. Walters
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- Journal:
- The British Journal of Psychiatry / Volume 216 / Issue 5 / May 2020
- Published online by Cambridge University Press:
- 03 June 2019, pp. 259-266
- Print publication:
- May 2020
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Background
Around 30% of individuals with schizophrenia remain symptomatic and significantly impaired despite antipsychotic treatment and are considered to be treatment resistant. Clinicians are currently unable to predict which patients are at higher risk of treatment resistance.
AimsTo determine whether genetic liability for schizophrenia and/or clinical characteristics measurable at illness onset can prospectively indicate a higher risk of treatment-resistant psychosis (TRP).
MethodIn 1070 individuals with schizophrenia or related psychotic disorders, schizophrenia polygenic risk scores (PRS) and large copy number variations (CNVs) were assessed for enrichment in TRP. Regression and machine-learning approaches were used to investigate the association of phenotypes related to demographics, family history, premorbid factors and illness onset with TRP.
ResultsYounger age at onset (odds ratio 0.94, P = 7.79 × 10−13) and poor premorbid social adjustment (odds ratio 1.64, P = 2.41 × 10−4) increased risk of TRP in univariate regression analyses. These factors remained associated in multivariate regression analyses, which also found lower premorbid IQ (odds ratio 0.98, P = 7.76 × 10−3), younger father's age at birth (odds ratio 0.97, P = 0.015) and cannabis use (odds ratio 1.60, P = 0.025) increased the risk of TRP. Machine-learning approaches found age at onset to be the most important predictor and also identified premorbid IQ and poor social adjustment as predictors of TRP, mirroring findings from regression analyses. Genetic liability for schizophrenia was not associated with TRP.
ConclusionsPeople with an earlier age at onset of psychosis and poor premorbid functioning are more likely to be treatment resistant. The genetic architecture of susceptibility to schizophrenia may be distinct from that of treatment outcomes.
Interaction between the FTO gene, body mass index and depression: meta-analysis of 13701 individuals
- Margarita Rivera, Adam E. Locke, Tanguy Corre, Darina Czamara, Christiane Wolf, Ana Ching-Lopez, Yuri Milaneschi, Stefan Kloiber, Sara Cohen-Woods, James Rucker, Katherine J. Aitchison, Sven Bergmann, Dorret I. Boomsma, Nick Craddock, Michael Gill, Florian Holsboer, Jouke-Jan Hottenga, Ania Korszun, Zoltan Kutalik, Susanne Lucae, Wolfgang Maier, Ole Mors, Bertram Müller-Myhsok, Michael J. Owen, Brenda W. J. H. Penninx, Martin Preisig, John Rice, Marcella Rietschel, Federica Tozzi, Rudolf Uher, Peter Vollenweider, Gerard Waeber, Gonneke Willemsen, Ian W. Craig, Anne E. Farmer, Cathryn M. Lewis, Gerome Breen, Peter McGuffin
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- Journal:
- The British Journal of Psychiatry / Volume 211 / Issue 2 / August 2017
- Published online by Cambridge University Press:
- 02 January 2018, pp. 70-76
- Print publication:
- August 2017
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Background
Depression and obesity are highly prevalent, and major impacts on public health frequently co-occur. Recently, we reported that having depression moderates the effect of the FTO gene, suggesting its implication in the association between depression and obesity.
AimsTo confirm these findings by investigating the FTO polymorphism rs9939609 in new cohorts, and subsequently in a meta-analysis.
MethodThe sample consists of 6902 individuals with depression and 6799 controls from three replication cohorts and two original discovery cohorts. Linear regression models were performed to test for association between rs9939609 and body mass index (BMI), and for the interaction between rs9939609 and depression status for an effect on BMI. Fixed and random effects meta-analyses were performed using METASOFT.
ResultsIn the replication cohorts, we observed a significant interaction between FTO, BMI and depression with fixed effects meta-analysis (β=0.12, P = 2.7 × 10−4) and with the Han/Eskin random effects method (P = 1.4 × 10−7) but not with traditional random effects (β = 0.1, P = 0.35). When combined with the discovery cohorts, random effects meta-analysis also supports the interaction (β = 0.12, P = 0.027) being highly significant based on the Han/Eskin model (P = 6.9 × 10−8). On average, carriers of the risk allele who have depression have a 2.2% higher BMI for each risk allele, over and above the main effect of FTO.
ConclusionsThis meta-analysis provides additional support for a significant interaction between FTO, depression and BMI, indicating that depression increases the effect of FTO on BMI. The findings provide a useful starting point in understanding the biological mechanism involved in the association between obesity and depression.
Postemergence herbicide application timing effects on annual grass control and corn (Zea mays) grain yield
- Larry S. Tapia, Thomas T. Bauman, Robert G. Harvey, James J. Kells, George Kapusta, Mark M. Loux, William E. Lueschen, Michael D. K. Owen, Larry H. Hageman, Stephen D. Strachan
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- Journal:
- Weed Science / Volume 45 / Issue 1 / February 1997
- Published online by Cambridge University Press:
- 12 June 2017, pp. 138-143
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Giant foxtail, woolly cupgrass, and wild-proso millet infest millions of hectares of land devoted to corn production in the midwestern U.S. Control of these species and effects on corn grain yield were evaluated at various timings using POST applications of nicosulfuron vs. applications of various PRE herbicides at 17 locations across the midwestern U.S. in 1992 and 1993. Nicosulfuron applied to 5 to 10 cm giant foxtail and woolly cupgrass provided greater control than that observed with selected PRE herbicides. Giant foxtail control with nicosulfuron averaged 88%, and control of woolly cupgrass averaged 77% across all sites. Nicosulfuron, applied to 5 to 10 cm wild-proso millet, provided a level of control similar to that of selected PRE herbicides. Corn grain yield was greater when giant foxtail was controlled POST with nicosulfuron vs. PRE control with selected soil-applied herbicides. Corn grain yields were similar when nicosulfuron was applied POST to 5 to 10 cm woolly cupgrass or wild-proso millet vs. PRE control of these grass weeds. Across a broad range of geographical locations, nicosulfuron, applied POST to 5 to 10 cm tall grass, provided greater or similar levels of weed control vs. the selected PRE herbicides, with no deleterious effect on grain yield.
A Multistate Study of the Association Between Glyphosate Resistance and EPSPS Gene Amplification in Waterhemp (Amaranthus tuberculatus)
- Laura A. Chatham, Kevin W. Bradley, Greg R. Kruger, James R. Martin, Micheal D. K. Owen, Dallas E. Peterson, Jugulam Mithila, Patrick J. Tranel
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- Journal:
- Weed Science / Volume 63 / Issue 3 / September 2015
- Published online by Cambridge University Press:
- 20 January 2017, pp. 569-577
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Waterhemp is an increasingly problematic weed in the U.S. Midwest, having now evolved resistances to herbicides from six different site-of-action groups. Glyphosate-resistant waterhemp in the Midwest is especially concerning given the economic importance of glyphosate in corn and soybean production. Amplification of the target-site gene, 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS) was found to be the mechanism of glyphosate resistance in Palmer amaranth, a species closely related to waterhemp. Here, the relationship between glyphosate resistance and EPSPS gene amplification in waterhemp was investigated. Glyphosate dose response studies were performed at field sites with glyphosate-resistant waterhemp in Illinois, Kansas, Kentucky, Missouri, and Nebraska, and relative EPSPS copy number of survivors was determined via quantitative real-time polymerase chain reaction (qPCR). Waterhemp control increased with increasing glyphosate rate at all locations, but no population was completely controlled even at the highest rate (3,360 g ae ha−1). EPSPS gene amplification was present in plants from four of five locations (Illinois, Kansas, Missouri, and Nebraska) and the proportion of plants with elevated copy number was generally higher in survivors from glyphosate-treated plots than in plants from the untreated control plots. Copy number magnitude varied by site, but an overall trend of increasing copy number with increasing rate was observed in populations with gene amplification, suggesting that waterhemp plants with more EPSPS copies are more resistant. Survivors from the Kentucky population did not have elevated EPSPS copy number. Instead, resistance in this population was attributed to the EPSPS Pro106Ser mutation. Results herein show a quantitative relationship between glyphosate resistance and EPSPS gene amplification in some waterhemp populations, while highlighting that other mechanisms also confer glyphosate resistance in waterhemp.
Assessment of Weed Control Strategies for Corn in the North-Central United States
- Brent E. Tharp, James J. Kells, Thomas T. Bauman, R. Gordon Harvey, William G. Johnson, Mark M. Loux, Alex R. Martin, Douglas J. Maxwell, Micheal D. K. Owen, David L. Regehr, Jon E. Warnke, Robert G. Wilson, Leon J. Wrage, Bryan G. Young, Caleb D. Dalley
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- Journal:
- Weed Technology / Volume 18 / Issue 2 / June 2004
- Published online by Cambridge University Press:
- 20 January 2017, pp. 203-210
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Field experiments were conducted across the north-central United States to determine the benefits of various weed control strategies in corn. Weed control, corn yield, and economic return increased when a preemergence (PRE) broad-spectrum herbicide was followed by (fb) postemergence (POST) herbicides. Weed control decisions based on field scouting after a PRE broad-spectrum herbicide application increased weed control and economic return. Application of a PRE grass herbicide fb a POST herbicide based on field scouting resulted in less control of velvetleaf and morningglory species, corn yield, and economic return compared with a PRE broad-spectrum herbicide application fb scouting. Cultivation after a PRE broad-spectrum herbicide application increased weed control and corn yield compared with the herbicide applied alone, but economic return was not increased. An early-postemergence herbicide application fb cultivation resulted in the highest level of broadleaf weed control, the highest corn yield, and the greatest economic return compared with all other strategies. Weed control based on scouting proved to be useful in reducing the effect of weed escapes on corn yield and increased economic return compared with PRE herbicide application alone. However, economic return was not greater than the PRE fb planned POST or total POST strategies.
The Origin and Evolution of Transition Discs: Successes, Problems, and Open Questions
- Part of
- James E. Owen
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- Journal:
- Publications of the Astronomical Society of Australia / Volume 33 / 2016
- Published online by Cambridge University Press:
- 15 February 2016, e005
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Transition discs are protoplanetary discs that show evidence for large holes or wide gaps (with widths comparable to their radii) in their dust component. These discs could be giving us clues about the disc destruction mechanism or hints about the location and time-scales for the formation of planets. However, at the moment there remain key gaps in our theoretical understanding. The vast majority of transition discs are accreting onto their central stars, indicating that—at least close to the star—dust has been depleted from the gas by a very large amount. In this review, we discuss evidence for two distinct populations of transition discs: mm-faint—those with low mm-fluxes, small holes (≲ 10 AU), and low accretion rates (~ 10−10 − 10−9 M⊙ yr−1) and mm-bright—discs with large mm-fluxes, large holes (≳ 20 AU), and high accretion rates ~ 10−8 M⊙ yr−1. MM-faint transition discs are consistent with what would naively be expected from a disc undergoing dispersal; however, mm-bright discs are not, and are likely to be rare and long-lived objects. We discuss the two commonly proposed mechanisms for creating transition discs: photoevaporation and planet–disc interactions, with a particular emphasis on how they would evolve in these models, comparing these predictions to the observed population. More theoretical work on explaining the lack of optically thick, non-accreting transition discs is required in both the photoevaporation and planetary hypothesis, before we can start to use transition discs to constrain models of planet formation. Finally, we suggest that the few discs with primordial looking spectral energy distribution, but serendipitously imaged showing large cavities in the mm (e.g. MWC758 and WSB 60) may represent a hidden population of associated objects. Characterising and understanding how these objects fit into the overall paradigm may allow us to unravel the mystery of transition discs.
Contributors
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- By Amr Abbasy, Mostafa I. Abuzeid, Omar M. Abuzeid, Gautam N. Allahbadia, Sarika Arora, Norman Assad, Awoniyi O. Awonuga, Osama M. Azmy, Shawky Z. A. Badawy, Haitham Badran, Jashoman Banerjee, M. N. Baumgarten, Donna C. Bennett, Josef Blankstein, Joel Brasch, Spyridon Chouliaras, Kathryn H. Clarke, Hans Peter Dietz, Jan Gerris, Harold Henning, Candice P. Holliday, Nicolette Holliday, Sadie Hutson, Kannamannadiar Jayaprakasan, Samuel Johnson, Salem K. Joseph, Asim Kurjak, John LaFleur, David F. Lewis, Kazuo Maeda, Rizwan Malik, Ehab Abu Marar, Rubina Merchant, Luciano G. Nardo, Geeta Nargund, Sheri A. Owens, Sree Durga Patchava, L. T. Polanski, Misty M. Blanchette Porter, Elizabeth E. Puscheck, Nicholas J. Raine-Fenning, Botros R. M. B. Rizk, Valerie Shavell, Osama Shawki, James Shwayder, Bruce Singer, Manvinder Singh, Beverly A. Spirt, Julie Sroga, Bradley J. Van Voorhis, Amr Hassan Wahba, Carrie Warshak, Terri L. Woodard
- Edited by Botros R. M. B. Rizk, University of South Alabama, Elizabeth E. Puscheck, Wayne State University, Detroit
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- Book:
- Ultrasonography in Gynecology
- Published online:
- 05 February 2015
- Print publication:
- 16 October 2014, pp xiii-xvi
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Analysis of copy number variations at 15 schizophrenia-associated loci
- Elliott Rees, James T. R. Walters, Lyudmila Georgieva, Anthony R. Isles, Kimberly D. Chambert, Alexander L. Richards, Gerwyn Mahoney-Davies, Sophie E. Legge, Jennifer L. Moran, Steven A. McCarroll, Michael C. O'Donovan, Michael J. Owen, George Kirov
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- Journal:
- The British Journal of Psychiatry / Volume 204 / Issue 2 / February 2014
- Published online by Cambridge University Press:
- 02 January 2018, pp. 108-114
- Print publication:
- February 2014
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Background
A number of copy number variants (CNVs) have been suggested as susceptibility factors for schizophrenia. For some of these the data remain equivocal, and the frequency in individuals with schizophrenia is uncertain.
AimsTo determine the contribution of CNVs at 15 schizophrenia-associated loci (a) using a large new data-set of patients with schizophrenia (n = 6882) and controls (n = 6316), and (b) combining our results with those from previous studies.
MethodWe used Illumina microarrays to analyse our data. Analyses were restricted to 520 766 probes common to all arrays used in the different data-sets.
ResultsWe found higher rates in participants with schizophrenia than in controls for 13 of the 15 previously implicated CNVs. Six were nominally significantly associated (P<0.05) in this new data-set: deletions at 1q21.1, NRXN1, 15q11.2 and 22q11.2 and duplications at 16p11.2 and the Angelman/Prader–Willi Syndrome (AS/PWS) region. All eight AS/PWS duplications in patients were of maternal origin. When combined with published data, 11 of the 15 loci showed highly significant evidence for association with schizophrenia (P<4.1×10−4).
ConclusionsWe strengthen the support for the majority of the previously implicated CNVs in schizophrenia. About 2.5% of patients with schizophrenia and 0.9% of controls carry a large, detectable CNV at one of these loci. Routine CNV screening may be clinically appropriate given the high rate of known deleterious mutations in the disorder and the comorbidity associated with these heritable mutations.
Notes on contributors
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- By James Eli Adams, Joseph Bristow, Oliver S. Buckton, Barbara Caine, Richard Cave, David Clifford, Harry Cocks, Matt Cook, Joseph Donohue, Richard Dorment, Sos Eltis, Helen Freshwater, Josephine M. Guy, Ellis Hanson, Merlin Holland, Russell Jackson, Jarlath Killeen, Leon Litvack, Ruth Livesey, Jerusha McCormack, Michèle Mendelssohn, Susan Owens, Kerry Powell, Steven Price, Peter Raby, Mark Ravenhill, John Paul Riquelme, Anthony Roche, Sean Ryder, Jan-Melissa Schramm, Ian Small, Philip E. Smith, Margaret D. Stetz, John Stokes, Mark W. Turner, Lynn Voskuil, Marcus Waithe
- Edited by Kerry Powell, Miami University, Peter Raby, Homerton College, Cambridge
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- Book:
- Oscar Wilde in Context
- Published online:
- 18 December 2013
- Print publication:
- 12 December 2013, pp xvi-xxii
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Contributors
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- By Rose Teteki Abbey, K. C. Abraham, David Tuesday Adamo, LeRoy H. Aden, Efrain Agosto, Victor Aguilan, Gillian T. W. Ahlgren, Charanjit Kaur AjitSingh, Dorothy B E A Akoto, Giuseppe Alberigo, Daniel E. Albrecht, Ruth Albrecht, Daniel O. Aleshire, Urs Altermatt, Anand Amaladass, Michael Amaladoss, James N. Amanze, Lesley G. Anderson, Thomas C. Anderson, Victor Anderson, Hope S. Antone, María Pilar Aquino, Paula Arai, Victorio Araya Guillén, S. Wesley Ariarajah, Ellen T. Armour, Brett Gregory Armstrong, Atsuhiro Asano, Naim Stifan Ateek, Mahmoud Ayoub, John Alembillah Azumah, Mercedes L. García Bachmann, Irena Backus, J. Wayne Baker, Mieke Bal, Lewis V. Baldwin, William Barbieri, António Barbosa da Silva, David Basinger, Bolaji Olukemi Bateye, Oswald Bayer, Daniel H. Bays, Rosalie Beck, Nancy Elizabeth Bedford, Guy-Thomas Bedouelle, Chorbishop Seely Beggiani, Wolfgang Behringer, Christopher M. Bellitto, Byard Bennett, Harold V. Bennett, Teresa Berger, Miguel A. Bernad, Henley Bernard, Alan E. Bernstein, Jon L. Berquist, Johannes Beutler, Ana María Bidegain, Matthew P. Binkewicz, Jennifer Bird, Joseph Blenkinsopp, Dmytro Bondarenko, Paulo Bonfatti, Riet en Pim Bons-Storm, Jessica A. Boon, Marcus J. Borg, Mark Bosco, Peter C. Bouteneff, François Bovon, William D. Bowman, Paul S. Boyer, David Brakke, Richard E. Brantley, Marcus Braybrooke, Ian Breward, Ênio José da Costa Brito, Jewel Spears Brooker, Johannes Brosseder, Nicholas Canfield Read Brown, Robert F. Brown, Pamela K. Brubaker, Walter Brueggemann, Bishop Colin O. Buchanan, Stanley M. Burgess, Amy Nelson Burnett, J. Patout Burns, David B. Burrell, David Buttrick, James P. Byrd, Lavinia Byrne, Gerado Caetano, Marcos Caldas, Alkiviadis Calivas, William J. Callahan, Salvatore Calomino, Euan K. Cameron, William S. Campbell, Marcelo Ayres Camurça, Daniel F. Caner, Paul E. Capetz, Carlos F. Cardoza-Orlandi, Patrick W. Carey, Barbara Carvill, Hal Cauthron, Subhadra Mitra Channa, Mark D. Chapman, James H. Charlesworth, Kenneth R. Chase, Chen Zemin, Luciano Chianeque, Philip Chia Phin Yin, Francisca H. Chimhanda, Daniel Chiquete, John T. Chirban, Soobin Choi, Robert Choquette, Mita Choudhury, Gerald Christianson, John Chryssavgis, Sejong Chun, Esther Chung-Kim, Charles M. A. Clark, Elizabeth A. Clark, Sathianathan Clarke, Fred Cloud, John B. Cobb, W. Owen Cole, John A Coleman, John J. Collins, Sylvia Collins-Mayo, Paul K. Conkin, Beth A. Conklin, Sean Connolly, Demetrios J. Constantelos, Michael A. Conway, Paula M. Cooey, Austin Cooper, Michael L. Cooper-White, Pamela Cooper-White, L. William Countryman, Sérgio Coutinho, Pamela Couture, Shannon Craigo-Snell, James L. Crenshaw, David Crowner, Humberto Horacio Cucchetti, Lawrence S. Cunningham, Elizabeth Mason Currier, Emmanuel Cutrone, Mary L. Daniel, David D. Daniels, Robert Darden, Rolf Darge, Isaiah Dau, Jeffry C. Davis, Jane Dawson, Valentin Dedji, John W. de Gruchy, Paul DeHart, Wendy J. 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Flowers, Carole Fontaine, David Ford, Mary Ford, Stephanie A. Ford, Jim Forest, William Franke, Robert M. Franklin, Ruth Franzén, Edward H. Friedman, Samuel Frouisou, Lorelei F. Fuchs, Jojo M. Fung, Inger Furseth, Richard R. Gaillardetz, Brandon Gallaher, China Galland, Mark Galli, Ismael García, Tharscisse Gatwa, Jean-Marie Gaudeul, Luis María Gavilanes del Castillo, Pavel L. Gavrilyuk, Volney P. Gay, Metropolitan Athanasios Geevargis, Kondothra M. George, Mary Gerhart, Simon Gikandi, Maurice Gilbert, Michael J. Gillgannon, Verónica Giménez Beliveau, Terryl Givens, Beth Glazier-McDonald, Philip Gleason, Menghun Goh, Brian Golding, Bishop Hilario M. Gomez, Michelle A. Gonzalez, Donald K. Gorrell, Roy Gottfried, Tamara Grdzelidze, Joel B. Green, Niels Henrik Gregersen, Cristina Grenholm, Herbert Griffiths, Eric W. Gritsch, Erich S. Gruen, Christoffer H. Grundmann, Paul H. Gundani, Jon P. Gunnemann, Petre Guran, Vidar L. Haanes, Jeremiah M. 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Phan, Isabel Apawo Phiri, William S. F. Pickering, Derrick G. Pitard, William Elvis Plata, Zlatko Plese, John Plummer, James Newton Poling, Ronald Popivchak, Andrew Porter, Ute Possekel, James M. Powell, Enos Das Pradhan, Devadasan Premnath, Jaime Adrían Prieto Valladares, Anne Primavesi, Randall Prior, María Alicia Puente Lutteroth, Eduardo Guzmão Quadros, Albert Rabil, Laurent William Ramambason, Apolonio M. Ranche, Vololona Randriamanantena Andriamitandrina, Lawrence R. Rast, Paul L. Redditt, Adele Reinhartz, Rolf Rendtorff, Pål Repstad, James N. Rhodes, John K. Riches, Joerg Rieger, Sharon H. Ringe, Sandra Rios, Tyler Roberts, David M. Robinson, James M. Robinson, Joanne Maguire Robinson, Richard A. H. Robinson, Roy R. Robson, Jack B. Rogers, Maria Roginska, Sidney Rooy, Rev. Garnett Roper, Maria José Fontelas Rosado-Nunes, Andrew C. Ross, Stefan Rossbach, François Rossier, John D. Roth, John K. Roth, Phillip Rothwell, Richard E. 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Stewart, Cynthia Stokes Brown, Ken Stone, Anne Stott, Elizabeth Stuart, Monya Stubbs, Marjorie Hewitt Suchocki, David Kwang-sun Suh, Scott W. Sunquist, Keith Suter, Douglas Sweeney, Charles H. Talbert, Shawqi N. Talia, Elsa Tamez, Joseph B. Tamney, Jonathan Y. Tan, Yak-Hwee Tan, Kathryn Tanner, Feiya Tao, Elizabeth S. Tapia, Aquiline Tarimo, Claire Taylor, Mark Lewis Taylor, Bishop Abba Samuel Wolde Tekestebirhan, Eugene TeSelle, M. Thomas Thangaraj, David R. Thomas, Andrew Thornley, Scott Thumma, Marcelo Timotheo da Costa, George E. “Tink” Tinker, Ola Tjørhom, Karen Jo Torjesen, Iain R. Torrance, Fernando Torres-Londoño, Archbishop Demetrios [Trakatellis], Marit Trelstad, Christine Trevett, Phyllis Trible, Johannes Tromp, Paul Turner, Robert G. Tuttle, Archbishop Desmond Tutu, Peter Tyler, Anders Tyrberg, Justin Ukpong, Javier Ulloa, Camillus Umoh, Kristi Upson-Saia, Martina Urban, Monica Uribe, Elochukwu Eugene Uzukwu, Richard Vaggione, Gabriel Vahanian, Paul Valliere, T. J. 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Yee, Viktor Yelensky, Yeo Khiok-Khng, Gustav K. K. Yeung, Angela Yiu, Amos Yong, Yong Ting Jin, You Bin, Youhanna Nessim Youssef, Eliana Yunes, Robert Michael Zaller, Valarie H. Ziegler, Barbara Brown Zikmund, Joyce Ann Zimmerman, Aurora Zlotnik, Zhuo Xinping
- Edited by Daniel Patte, Vanderbilt University, Tennessee
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- The Cambridge Dictionary of Christianity
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- 05 August 2012
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- 20 September 2010, pp xi-xliv
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Looking Backward, Looking Forward: MLA Members Speak
- April Alliston, Elizabeth Ammons, Jean Arnold, Nina Baym, Sandra L. Beckett, Peter G. Beidler, Roger A. Berger, Sandra Bermann, J.J. Wilson, Troy Boone, Alison Booth, Wayne C. Booth, James Phelan, Marie Borroff, Ihab Hassan, Ulrich Weisstein, Zack Bowen, Jill Campbell, Dan Campion, Jay Caplan, Maurice Charney, Beverly Lyon Clark, Robert A. Colby, Thomas C. Coleman III, Nicole Cooley, Richard Dellamora, Morris Dickstein, Terrell Dixon, Emory Elliott, Caryl Emerson, Ann W. Engar, Lars Engle, Kai Hammermeister, N. N. Feltes, Mary Anne Ferguson, Annie Finch, Shelley Fisher Fishkin, Jerry Aline Flieger, Norman Friedman, Rosemarie Garland-Thomson, Sandra M. Gilbert, Laurie Grobman, George Guida, Liselotte Gumpel, R. K. Gupta, Florence Howe, Cathy L. Jrade, Richard A. Kaye, Calhoun Winton, Murray Krieger, Robert Langbaum, Richard A. Lanham, Marilee Lindemann, Paul Michael Lützeler, Thomas J. Lynn, Juliet Flower MacCannell, Michelle A. Massé, Irving Massey, Georges May, Christian W. Hallstein, Gita May, Lucy McDiarmid, Ellen Messer-Davidow, Koritha Mitchell, Robin Smiles, Kenyatta Albeny, George Monteiro, Joel Myerson, Alan Nadel, Ashton Nichols, Jeffrey Nishimura, Neal Oxenhandler, David Palumbo-Liu, Vincent P. Pecora, David Porter, Nancy Potter, Ronald C. Rosbottom, Elias L. Rivers, Gerhard F. Strasser, J. L. Styan, Marianna De Marco Torgovnick, Gary Totten, David van Leer, Asha Varadharajan, Orrin N. C. Wang, Sharon Willis, Louise E. Wright, Donald A. Yates, Takayuki Yokota-Murakami, Richard E. Zeikowitz, Angelika Bammer, Dale Bauer, Karl Beckson, Betsy A. Bowen, Stacey Donohue, Sheila Emerson, Gwendolyn Audrey Foster, Jay L. Halio, Karl Kroeber, Terence Hawkes, William B. Hunter, Mary Jambus, Willard F. King, Nancy K. Miller, Jody Norton, Ann Pellegrini, S. P. Rosenbaum, Lorie Roth, Robert Scholes, Joanne Shattock, Rosemary T. VanArsdel, Alfred Bendixen, Alarma Kathleen Brown, Michael J. Kiskis, Debra A. Castillo, Rey Chow, John F. Crossen, Robert F. Fleissner, Regenia Gagnier, Nicholas Howe, M. Thomas Inge, Frank Mehring, Hyungji Park, Jahan Ramazani, Kenneth M. Roemer, Deborah D. Rogers, A. LaVonne Brown Ruoff, Regina M. Schwartz, John T. Shawcross, Brenda R. Silver, Andrew von Hendy, Virginia Wright Wexman, Britta Zangen, A. Owen Aldridge, Paula R. Backscheider, Roland Bartel, E. M. Forster, Milton Birnbaum, Jonathan Bishop, Crystal Downing, Frank H. Ellis, Roberto Forns-Broggi, James R. Giles, Mary E. Giles, Susan Blair Green, Madelyn Gutwirth, Constance B. Hieatt, Titi Adepitan, Edgar C. Knowlton, Jr., Emanuel Mussman, Sally Todd Nelson, Robert O. Preyer, David Diego Rodriguez, Guy Stern, James Thorpe, Robert J. Wilson, Rebecca S. Beal, Joyce Simutis, Betsy Bowden, Sara Cooper, Wheeler Winston Dixon, Tarek el Ariss, Richard Jewell, John W. Kronik, Wendy Martin, Stuart Y. McDougal, Hugo Méndez-Ramírez, Ivy Schweitzer, Armand E. Singer, G. Thomas Tanselle, Tom Bishop, Mary Ann Caws, Marcel Gutwirth, Christophe Ippolito, Lawrence D. Kritzman, James Longenbach, Tim McCracken, Wolfe S. Molitor, Diane Quantic, Gregory Rabassa, Ellen M. Tsagaris, Anthony C. Yu, Betty Jean Craige, Wendell V. Harris, J. Hillis Miller, Jesse G. Swan, Helene Zimmer-Loew, Peter Berek, James Chandler, Hanna K. Charney, Philip Cohen, Judith Fetterley, Herbert Lindenberger, Julia Reinhard Lupton, Maximillian E. Novak, Richard Ohmann, Marjorie Perloff, Mark Reynolds, James Sledd, Harriet Turner, Marie Umeh, Flavia Aloya, Regina Barreca, Konrad Bieber, Ellis Hanson, William J. Hyde, Holly A. Laird, David Leverenz, Allen Michie, J. Wesley Miller, Marvin Rosenberg, Daniel R. Schwarz, Elizabeth Welt Trahan, Jean Fagan Yellin
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- Journal:
- PMLA / Publications of the Modern Language Association of America / Volume 115 / Issue 7 / December 2000
- Published online by Cambridge University Press:
- 23 October 2020, pp. 1986-2078
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- December 2000
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Oestrogen uptake and metabolism in vivo
- V. H. T. James, M. J. Reed, E. F. Adams, M. Ghilchick, L. C. Lai, N. G. Coldham, C. J. Newton, A. Purohit, A. M. Owen, A. Singh, S. Islam
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- Journal:
- Proceedings of the Royal Society of Edinburgh. Section B: Biological Sciences / Volume 95 / 1989
- Published online by Cambridge University Press:
- 05 December 2011, pp. 185-193
- Print publication:
- 1989
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Uptake of oestrogens into breast tissue and their subsequent metabolism can be studied by infusing radio-labelled steroids into volunteer patients. Such studies show that oestradiol is preferentially accumulated in breast tumours, oestradiol concentrations exceeding those of oestrone. This contrasts with plasma, in which oestrone concentrations in postmenopausal women are greater than those of the oestradiol. This observation suggests that tissue factors can modulate local oestrogen metabolism, and thus local steroid concentrations.
We have studied the local production of oestrogens from androgen, and also the interconversion of the major oestrogens, oestrone and oestradiol. Using isotopic techniques, it is possible to calculate the proportion of endogenous oestrogen produced from androgen, as opposed to uptake from the circulation. These studies suggest that a very variable proportion of tissue oestrogen derives from endogenous synthesis. After administration of aromatase inhibitors, aromatase activity is substantially inhibited, both in vivo and in vitro.
Relative oestrogen concentrations are determined in part by the activity of oestradiol dehydrogenase. In breast tissue, dehydrogenase activity is present and this is modified by various factors, including androgens. In addition, we have demonstrated that normal, benign and malignant breast tissues produce factors which can modulate both growth and dehydrogenase activity of cancer cells in vitro.
We conclude that breast tissue is a site of synthesis of oestrogens, and that a number of factors can affect their local concentration. Tumour cells produce growth factors which can influence steroid metabolism, and may thus be able to enhance favourably their own endocrine environment.
X-ray Fluorescence Analysis of Trace Metals in the Annual Growth Layers of Freshwater Mussel Shells
- William E. Maddox, Leon Duobinis-Gray, David A. Owen, James B. Sickel
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- Journal:
- Advances in X-ray Analysis / Volume 33 / 1989
- Published online by Cambridge University Press:
- 06 March 2019, pp. 665-670
- Print publication:
- 1989
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Freshwater mussels (Mollusca: Unionidae) are filter feeders that are relatively immobile, widely distributed and are known to concentrate trace metals in their shells (1,2,3). These characteristics make them good candidates for monitoring metal pollution in lakes and rivers. Another characteristic of mussels that make them particularly attractive as pollution monitors is the fact the shell is deposited in distinctive, annual growth layers. The concentrations of metals in these shell layers may provide a history ol the metals present in the environment where the mussel was collected.
Do Operant Treatments of Chronic Pain Adhere to Precepts of Behavioural Analysis?
- Drifa Hardardottir, Jack E. James, Neville Owen
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- Journal:
- Behavioural and Cognitive Psychotherapy / Volume 16 / Issue 3 / July 1988
- Published online by Cambridge University Press:
- 16 June 2009, pp. 153-164
- Print publication:
- July 1988
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Fordyce's (1976) analysis of pain behaviour provides a framework for evaluating the extent to which empirical studies of the operant treatment of chronic pain have adhered to appropriate behaviour–analytic principles. These are the identification of target behaviours and their reinforcing contingencies, the specification of individualised reinforcers to be used in treatment, and the generalisation and maintenance of treatment effects. Twenty-five studies that reported having used an operant approach in the management of chronic pain problems were reviewed. With one exception, none of the studies reported sufficient data to indicate the degree of adherence to behaviour–analytic principles. Until more such data are reported, it will continue to be difficult to determine clearly those factors that contribute to the efficacy of operant approaches to chronic pain management.