Institution
Warneford Hospital
Healthcare•Oxford, United Kingdom•
About: Warneford Hospital is a healthcare organization based out in Oxford, United Kingdom. It is known for research contribution in the topics: Poison control & Population. The organization has 762 authors who have published 1396 publications receiving 105628 citations. The organization is also known as: Oxford Lunatic Asylum & Radcliffe Lunatic Asylum.
Topics: Poison control, Population, Eating disorders, Anxiety, Bipolar disorder
Papers published on a yearly basis
Papers
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TL;DR: Although the two measures performed similarly with respect to the assessment of unambiguous behavioral features such as self-induced vomiting and dieting, the self-report questionnaire generated higher scores than the interview when assessing more complex featuressuch as binge eating and concerns about shape.
Abstract: A detailed comparison was made of two methods for assessing the features of eating disorders. An investigator-based interview was compared with a self-report questionnaire based directly on that interview. A number of important discrepancies emerged. Although the two measures performed similarly with respect to the assessment of unambiguous behavioral features such as self-induced vomiting and dieting, the self-report questionnaire generated higher scores than the interview when assessing more complex features such as binge eating and concerns about shape. Both methods underestimated body weight.
4,250 citations
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TL;DR: A new transdiagnostic theory of the maintenance of the full range of eating disorders is proposed, a theory which embraces a broader range of maintaining mechanisms than the current theory concerning bulimia nervosa.
2,659 citations
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TL;DR: A meta-analytic review of cross-sectional studies of the association of peer victimization with psychosocial maladjustment suggested that victimization is most strongly related to depression, and least stronglyrelated to anxiety.
Abstract: Cross-sectional quantitative designs are often used to investigate whether peer victimization is positively related to psychosocial maladjustment. This paper presents a meta-analytic review of cross-sectional studies, published between 1978 and 1997, of the association of peer victimization with psychosocial maladjustment. Mean effect sizes were calculated for the association between peer victimization and each form of maladjustment (depression, loneliness, generalized and social anxiety, and global and social self-worth) assessed. The results suggested that victimization is most strongly related to depression, and least strongly related to anxiety. There was no evidence that victimization is more strongly related to social than to psychological forms of maladjustment. Effect sizes were stronger when the same informants were used to assess both victimization and maladjustment than when different informants were used. There were some design limitations to the studies reviewed, but all together their results provide a strong background for more complex research into the course and treatment of victims' distress.
2,603 citations
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Oxford Health NHS Foundation Trust1, University of Oxford2, Kyoto University3, University of Bern4, Cochrane Collaboration5, Sorbonne6, Paris Descartes University7, Warneford Hospital8, Technische Universität München9, Radboud University Nijmegen Medical Centre10, Oregon Health & Science University11, University of Bristol12, Stanford University13
TL;DR: This work aimed to update and expand previous work to compare and rank antidepressants for the acute treatment of adults with unipolar major depressive disorder, and found that all antidepressants were more effective than placebo.
1,697 citations
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TL;DR: Functional imaging data indicate that the pathophysiology of schizophrenia reflects aberrant activity in, and integration of, the components of distributed circuits involving the prefrontal cortex, hippocampus and certain subcortical structures.
Abstract: Despite a hundred years' research, the neuropathology of schizophrenia remains obscure. However, neither can the null hypothesis be sustained--that it is a 'functional' psychosis, a disorder with no structural basis. A number of abnormalities have been identified and confirmed by meta-analysis, including ventricular enlargement and decreased cerebral (cortical and hippocampal) volume. These are characteristic of schizophrenia as a whole, rather than being restricted to a subtype, and are present in first-episode, unmedicated patients. There is considerable evidence for preferential involvement of the temporal lobe and moderate evidence for an alteration in normal cerebral asymmetries. There are several candidates for the histological and molecular correlates of the macroscopic features. The probable proximal explanation for decreased cortical volume is reduced neuropil and neuronal size, rather than a loss of neurons. These morphometric changes are in turn suggestive of alterations in synaptic, dendritic and axonal organization, a view supported by immunocytochemical and ultrastructural findings. Pathology in subcortical structures is not well established, apart from dorsal thalamic nuclei, which are smaller and contain fewer neurons. Other cytoarchitectural features of schizophrenia which are often discussed, notably entorhinal cortex heterotopias and hippocampal neuronal disarray, remain to be confirmed. The phenotype of the affected neuronal and synaptic populations is uncertain. A case can be made for impairment of hippocampal and corticocortical excitatory pathways, but in general the relationship between neurochemical findings (which centre upon dopamine, 5-hydroxytryptamine, glutamate and GABA systems) and the neuropathology of schizophrenia is unclear. Gliosis is not an intrinsic feature; its absence supports, but does not prove, the prevailing hypothesis that schizophrenia is a disorder of prenatal neurodevelopment. The cognitive impairment which frequently accompanies schizophrenia is not due to Alzheimer's disease or any other recognized neurodegenerative disorder. Its basis is unknown. Functional imaging data indicate that the pathophysiology of schizophrenia reflects aberrant activity in, and integration of, the components of distributed circuits involving the prefrontal cortex, hippocampus and certain subcortical structures. It is hypothesized that the neuropathological features represent the anatomical substrate of these functional abnormalities in neural connectivity. Investigation of this proposal is a goal of current neuropathological studies, which must also seek (i) to establish which of the recent histological findings are robust and cardinal, and (ii) to define the relationship of the pathological phenotype with the clinical syndrome, its neurochemistry and its pathogenesis.
1,648 citations
Authors
Showing all 770 results
Name | H-index | Papers | Citations |
---|---|---|---|
Paul Harrison | 133 | 1400 | 80539 |
Keith Hawton | 125 | 657 | 55138 |
Christopher G. Fairburn | 113 | 343 | 51987 |
Guy M. Goodwin | 109 | 580 | 43407 |
David M. Clark | 102 | 370 | 40943 |
Graham Dunn | 101 | 484 | 37152 |
Simon Lovestone | 98 | 564 | 45767 |
Luke Clark | 90 | 250 | 23015 |
Derick T Wade | 90 | 398 | 37413 |
Anna C. Nobre | 86 | 316 | 27847 |
Philip J. Cowen | 85 | 506 | 28107 |
Michael Sharpe | 84 | 417 | 30546 |
Anke Ehlers | 84 | 289 | 31400 |
Daniel Freeman | 83 | 385 | 22990 |
John R. Geddes | 83 | 441 | 37064 |