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The Line between Psychosis and Schizotypy: a case report
- L. Huerga García, E. Hernández Padrón, N. Casanova Gracia, N. Torres Nieves, P. Gómez Pérez, F. Garcia Gómez-Pamo, J.J. Dorta Gonzalez, J.F. Dorta González
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- Journal:
- European Psychiatry / Volume 65 / Issue S1 / June 2022
- Published online by Cambridge University Press:
- 01 September 2022, p. S437
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Introduction
Since Kraepelin and Bleuler, schizotypy was understood as a mild expression of psychosis, a latent form with the same trajectory but different severity. They pointed characteristics such as being eccentric, unreasonable, supersticious or hipersensitive, interpersonal aversiveness (often related to suspiciousness and expectation of rejection), ambivalence, anhedonia,… and psychosis-like features that don’t usually lead to help-seeking.
ObjectivesTo do a case review
MethodsWe report a case of a 17 years old boy with a childhood trauma history who started psychiatric consultations a year and a half ago because his “usual” (as his mother referred) strange behaviour got worse, which was perceived by his
ENT specialist. During the appointments, the patient showed suspiciousness, odd speech, inappropriate affect, tendency to social withdrawal, obsessive ruminations with sexual content and occasional perceptual experiences (such as depersonalization, derealization and auditory hallucinations).
ResultsPsychosis and schizotypy are linked historically and phenomenologically, which is evidenced by their placement in non-affective psychosis in the ICD-10 and DSM-5, and it is known that the direct observation (by clinicians or family members) during the childhood and adolescence are key for a correct diagnosis. In fact, this construct reflects a phenotypic expression of vulnerability to schizophrenia, and during childhood or adolescence it may be understood as an early mental risk state.
ConclusionsIn contrast to models of psychosis that mainly rely on positive features and assume a progression of them, the positive traits of schizotypy seem to be beneficial and related to a “benign or happy schizotypy” according to the articles we reviewed.
DisclosureNo significant relationships.
OCD and ASD Diagnosis: a case review
- L. Huerga García, E. Hernández Padrón, N. Casanova Gracia, N. Torres Nieves, P. Gómez Pérez
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- Journal:
- European Psychiatry / Volume 65 / Issue S1 / June 2022
- Published online by Cambridge University Press:
- 01 September 2022, p. S392
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Introduction
It’s well known the challenge of differential diagnosis between Obssesive compulsive disorder and autism since their symptoms (intrusive, recurrent thoughts and repetitive behaviours) often overlap.
ObjectivesWe report a case of a 14 years old boy diagnosed of ASD who was hospitalized for the first time due to difficult management of repetitive behaviours that made him incapable of doing basic activities without help. To interrupt them led to anxiety, aggressive responses and to insistence on sameness behaviours. Only with this information and with the literature research we made, anyone could tell the problem was probably an ASD symptom. However, during his evolution it was difficult to know whether this behaviour was due to ASD or OCD: after adjusting the medication, and when he started trusting his therapists, he told us about a theory he believed so he could explain the uncomfortable ideas that crossed his mind more than often, so he used those behaviours as an anxiety-reduction technique. This new situation was the fuel to make the present review.
MethodsTo report a case.
ResultsThe results are included in the “conclusions” section.
ConclusionsAlthough there is an ongoing debate concerning the nature of the symptoms in ASD versus those observed in OCD, there are commonly used criteria to differentiate them according to the articles we reviewed:
DisclosureNo significant relationships.
Chronic agomelatine administration modulates neuronal plasticity markers in the rat prefrontal cortex, hippocampus and amygdala
- N. Ladurelle, C. Potard, C. Gabriel-Gracia, E. Mocaër, E. Beaulieu, M. Bianchi
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- Journal:
- European Psychiatry / Volume 26 / Issue S2 / March 2011
- Published online by Cambridge University Press:
- 16 April 2020, p. 652
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Neuronal plasticity alterations including cytoskeletal dynamics and synaptic markers have been recently associated with the treatment of major depression. Here we investigated the effects of agomelatine, a novel antidepressant with melatonergic (MT1/MT2) agonist and 5-HT2C receptor antagonist properties, on cytoskeletal microtubular proteins and synaptic markers in the rat hippocampus, prefrontal cortex (PFC) and amygdala.
Adult male Sprague Dawley rats received daily i.p. administration of hydroxyethylcellulose 1% (vehicle) or agomelatine (40mg/kg) for 22 days. The rats were then sacrificed and hippocampi, PFC and amygdala dissected for analyses of microtubule dynamics markers (Tyr/Glu-Tub, Delta2-Tub and Acet-Tub) and synaptic markers (synaptophysin, PSD-95 and spinophilin) by Western blot.
In the PFC, agomelatine decreased Tyr/Glu-Tub and the neuronal-specific Delta2-Tub, suggesting decreased microtubule dynamics. In contrast, in the hippocampus Tyr/Glu-Tub and Delta2-Tub were increased, indicative of enhanced microtubule dynamics. A similar pattern to those seen in the hippocampus, but of higher magnitude, was observed in the amygdala where an important increase of Tyr/Glu-Tub accompanied by a decrease of the stable form Acet-Tub was observed. These findings were paralleled by decreased hippocampal spinophilin (dendritic spines marker), increased synaptophysin (pre-synaptic marker) and spinophilin in the PFC and amygdala and increased PSD-95 (post-synaptic marker) in the amygdala, all consistent with synaptic remodelling phenomena.
Taken together, these data shown that chronic agomelatine induces a differential modulation of microtubule dynamics and synaptic markers in the rat hippocampus, PFC and amygdala. These findings may have a particular relevance considering the fundamental role of these three brain areas in depression.
Electroconvulsive Therapy in Treatment-Resistant Schizophrenia: a Case Report
- V.M. Barrau, M. Salinas, S. Yelmo, E. Santana, F. Montiano, N. Gallego, G. Bello, R. Gracia
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- European Psychiatry / Volume 26 / Issue S2 / March 2011
- Published online by Cambridge University Press:
- 16 April 2020, p. 1135
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Electroconvulsive therapy (ECT) is born as we know it in the first half of the twentieth century. Although initially introduced as a treatment for schizophrenia, soon proved more effective in affective disorders.
Currently this therapy is second choice in the treatment of schizophrenia, representing only 10–20% of ECT treatments.
We present a 55 years-old-woman diagnosed with Paranoid Schizophrenia in the adolescence, with several hospital admissions who was sent from sub-acute unit to receive ECT, given the null response to several pharmacological trials. The last, 1,200 mg amisulpride, 650 mg clozapine and 1,000 mg valproate per day, and Zuclopenthixol ampoule every 14 days. She verbalizes poorly structured persecutory, megalomaniac and nihilist delusional ideas, as well as auditory hallucinations which she does not clarify, and thought broadcasting phenomena. After withdrawing this medication and starting treatment with 30 mg haloperidol and 550 mg quetiapine, 14 bifrontotemporal ECT sessions were given.
Given the disappearance of persecutory delusional ideas, and the decrease of auditory hallucinations, which she criticizes, the patient was discharged. After 4 months, she is still psychopathologically stable, and receiving maintenance ECT biweekly.
ECT, either alone or in combination with conventional antipsychotic drugs, has been shown effective in a certain percentage of patients with acute schizophrenia, particularly in the catatonic subtype and also in schizoaffective disorder. The use and efficacy of ECT in chronic schizophrenia is a more controversial topic.
Research should also focus on the determination of optimal number of ECT, the predictors of response and the efficacy of continuation and maintenance ECT.
2179 – Psychedelic Drugs In Psychotherapy. a Revival?
- V.M. Barrau-Alonso, J. Sendra-Lopez, N. Benítez-Álvarez, E. Vera-Barrios, A. Hernández-Dorta, G. Díaz-Marrero, I. González, P. Quandt, R. Gracia-Marco
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- European Psychiatry / Volume 28 / Issue S1 / 2013
- Published online by Cambridge University Press:
- 15 April 2020, 28-E1342
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Introduction
Psychedelic drugs were used extensively in psychotherapy in the 1950s to lower psychological defences and facilitate emotional insight. Thousands of research participants were administered hallucinogens in the context of basic clinical research or therapeutic clinical research, resulting in hundreds of publications. Results across studies were ultimately inconclusive due to such variations in methods and a lack of modern controls and experimental rigour. The growing controversy and sensationalism resulted in increasing restrictions on access to hallucinogens throughout the 1960s (ultimately resulting in the placement of the most popular hallucinogens into Schedule I of the 1970 Controlled Substances Act in the United States).
AimsRenewed human administration research began in the 1990s. Recent clinical studies have administered hallucinogens to evaluate their safety and efficacy in the treatment of psychiatric disorders: specifically, anxiety related to advanced-stage cancer (Grob, 2005), obsessive-compulsive disorder (Moreno, et al., 2006), heroin dependence (Krupitsky, et al., 2007), personal meaning and spiritual significance (Griffiths, et al., 2008), and a meta-analysis of randomized controlled trials of LSD for alcoholism (Krebs,et al., 2012).
ResultsPsychedelic-assisted psychotherapy utilizes the acute psychological effects of psychedelic drugs to enhance the normal mechanisms of psychotherapy. The effects of psychedelic psychotherapy are often very pronounced within several days or weeks after a treatment session, but then these effects quickly decline. This phenomenon was termed a “psychedelic afterglow”.
ConclusionsFhurther research, blinded, randomized, placebo-controlled, methodology should explore the efficacy of hallucinogens.
EPA-0294 – Can Alpha 1 Glycoproptein be Considered as a Marker of Negative Symptoms in Schizophrenia Patients?
- M. Henry-Benitez, A. Morera-Fumero, A. Henry-Gonzalez, A. Garcìa-Hernandez, L. Fernandez-Lopez, E. Diaz-Mesa, S. Yelmo-Cruz, C. Casariego-Ramìrez, N. Suarez-Benitez, R. Gracia-Marco, J. Monzon-Diaz, J.P. Girbau-Ronda
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- European Psychiatry / Volume 29 / Issue S1 / 2014
- Published online by Cambridge University Press:
- 15 April 2020, p. 1
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Introduction:
Recently, a renaissance of interest in ‘negative symptoms’ as emotional withdrawal or blunted affect, has occurred. Some investigators believe that these symptoms are important indicators of outcome, of response to treatment and of a distinct underlying pathologic process.
Research on the negative-symptom syndrome in schizophrenia has been handicapped until recently.
Aims:This research aims at studying whether acute phase proteins, precisely, Alpha1-glycoprotein, can be considered as a marker of negativesymptom in Schizophrenia.
Methods:29 chronic schizophrenics were assessed by the Positive and Negative Syndrome Scale (PANSS). A routine blood test including Alpha1-glycoprotein levels was carried out.
Results:Alpha1-glycoprotein shows a positive correlation, according to Pearson correlation coefficient, with the Negative Scale at an almost significant level (p=.05), and at a significant level in the following items, Blunted affect (p=.03), Passive/apathetic Social Withdrawal (p=.01) of the Negative spectrum and Poor Attention (p=.02) of the General Psychopathology Scale.
Conclusions:There is a significant correlation with two Negative variables and an almost significant one, spite of the small sample, with the Negative Scale. Further studies with bigger samples are needed in order to consider alpha1-glycoprotein as a schizophrenia negative psychopathology marker.
P-941 - Factor Structure of the Mcmi-iii in a Psychiatric Patients Sample
- M. Salinas, E. Santana, J. Chico, V. Barrau, S. Yelmo, N. Gallego, S. Poyo, R. Gracia
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- Journal:
- European Psychiatry / Volume 27 / Issue S1 / 2012
- Published online by Cambridge University Press:
- 15 April 2020, p. 1
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Introduction
The convenience of a dimensional Axis II in the DSM-5 has been discussed, since there is criticism about the current categorical model, such as the high comorbidity or the scarce interrater agreement. Some think that those flaws could be attributed to the lack of an underlying theoretical model. To this respect, there are evidences that show that the personality disorders could be considered as extreme cases of normal personality traits. We try to find out if the factor analysis of a personality disorder scale (MCMI-III) reflects normal personality factors.
MethodParticipants and procedure: we analyzed the MCMI-III (Millon, 1998) profiles of 50 Personality Disorders patients and 50 controls. Principal Components Factor Analyses with varimax rotation were computed globally and separately for each sample.
ResultsA three factor structure (paranoid introversion, self control and insecurity) was found when analyzing both samples together. The separated samples analysis showed the same structure in controls, while in patients we found a three factor structure: neurotic introversion, hostility and self control. Both structures were basically equivalent, and differences among them could be qualified by a test bias (namely, higher averages for patients in the anxious and psychotic-like disorders).
ConclusionsFactor structures did not reflect the DSM-IV cluster division, and neither did it reflect Millon's classification. Conversely, the factors we found were consistent with personality traits previously described by normal personality models (e.g.: Cattell, 1957; Costa y McCrae, 1990; Eysenck, 1981).
EPA-0356 – Tuberous Esclerosis Complex and Psychiatric Comorbidity: Two Case Reports
- J. Suarez-Jesus, S. Yelmo-Cruz, D. Paico-Rodriguez, N. Suarez-Benitez, G. Diaz-Marrero, M. Henry-Benitez, R. Gracia-Marco
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- European Psychiatry / Volume 29 / Issue S1 / 2014
- Published online by Cambridge University Press:
- 15 April 2020, p. 1
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Introduction:
Tuberous Sclerosis Complex (TSC) is a genetic inherited disease characterized by hamartomatous growths in several organs as brain, skin, kidneys, hearth and eyes. The estimated incidence is approximately 1:6000 live births. The diagnosis is made clinically. Seizures are present in 87% of patients. Psychiatric comorbidity has been reported.
Objectives:We report the clinical course of two patients with previous diagnosis of TSC. Psychiatric symptoms start in the adulthood without seizures history and absence of Subependimal Giant Cells Tumor (SGCT). The evolution and clinical features are described.
Methods:Patient 1
Married 33-years-old woman with two children affected with TSC. She was diagnosed after headache presentation in 2011. Initial MRI showed periventricular glioneuronal hamartomas. In January 2013 start with self-injurious (swallowing of objects) and autistic behaviours as well as several hospital urgency room visits. In addition, the patient presented with dull mood, emotional indifference and intellectual impairment, with no response to medication.
Patient 2
Married 43-years-old woman with a daughter affected with TSC. Diagnosis was made in 1999 and psychotic symptoms (delusional beliefs and auditory hallucinations) started in 2011 without previous psychiatric history. The MRI in 2013 shown subependymal nodules. Treatment with risperidone was effective.
Results:Psychiatric symptoms are very often associated to the physical findings on TSC, even in adulthood diagnoses.
Conclusions:Psychiatric comorbidities are well described in literature. about 10-20% adult patients with TSC present clinically significant behavioral problems as self-injuries, frequently associated with SGCT. The European Expert Panel recommended regular assessment of cognitive development and behaviour and symptomatic treatment.
S126 Invited—Residual Stress Measurements on Thin Films with a Focused Ion Beam Equipment
- N. Sabaté, C. Cané, I. Gràcia, D. Vogel, A. Gollhardt, B. Michel, K. J. Kang
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- Journal:
- Powder Diffraction / Volume 23 / Issue 2 / June 2008
- Published online by Cambridge University Press:
- 20 May 2016, p. 184
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Staging cognitive impairment and incidence of dementia
- J. Santabárbara, R. Lopez-Anton, P. Gracia-García, C. De-la-Cámara, D. Vaquero-Puyuelo, E. Lobo, G. Marcos, L. Salvador-Carulla, T. Palomo, N. Sartorius, A. Lobo
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- Epidemiology and Psychiatric Sciences / Volume 25 / Issue 6 / December 2016
- Published online by Cambridge University Press:
- 15 October 2015, pp. 562-572
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Aims.
In a background of interest in staging models in psychiatry, we tested the validity of a simple staging model of cognitive impairment to predict incident dementia.
Method.A large community sample of adults aged ≥55 years (N = 4803) was assessed in the baseline of a longitudinal, four-wave epidemiological enquiry. A two-phase assessment was implemented in each wave, and the instruments used included the Mini-Mental Status Examination (MMSE); the History and Aetiology Schedule and the Geriatric Mental State-AGECAT. For the standardised degree of cognitive impairment Perneczky et al's MMSE criteria were applied. A panel of psychiatrists diagnosed cases of dementia according to DSM-IV criteria, and cases and sub-cases of dementia were excluded for the follow-up waves. Competing risk regression models, adjusted by potential confounders, were used to test the hypothesised association between MMSE levels and dementia risk.
Results.Out of the 4057 participants followed up, 607 (14.9%) were classified as ‘normal’ (no cognitive impairment), 2672 (65.8%) as ‘questionable’ cognitive impairment, 732 (18.0%) had ‘mild’ cognitive impairment, 38 (0.9%) had ‘moderate’ cognitive impairment and eight (0.2%) had ‘severe’ impairment.
Cognitive impairment was associated with risk of dementia, the risk increasing in parallel with the level of impairment (hazard ratio: 2.72, 4.78 and 8.38 in the ‘questionable’, ‘mild’ and ‘moderate’ level of cognitive impairment, respectively).
Conclusions.The documented gradient of increased risk of dementia associated with the severity level of cognitive impairment supports the validity of the simple staging model based on the MMSE assessment.
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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Degree of cognitive impairment and mortality: a 17-year follow-up in a community study
- J. Santabárbara, R. Lopez-Anton, G. Marcos, C. De-la-Cámara, E. Lobo, P. Saz, P. Gracia-García, T. Ventura, A. Campayo, L. Rodríguez-Mañas, B. Olaya, J. M. Haro, L. Salvador-Carulla, N. Sartorius, A. Lobo
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- Epidemiology and Psychiatric Sciences / Volume 24 / Issue 6 / December 2015
- Published online by Cambridge University Press:
- 06 June 2014, pp. 503-511
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Background.
To test the hypothesis that cognitive impairment in older adults is associated with all-cause mortality risk and the risk increases when the degree of cognitive impairment augments; and then, if this association is confirmed, to report the population-attributable fraction (PAF) of mortality due to cognitive impairment.
Method.A representative random community sample of individuals aged over 55 was interviewed, and 4557 subjects remaining alive at the end of the first year of follow-up were included in the analysis. Instruments used in the assessment included the Mini-Mental Status Examination (MMSE), the History and Aetiology Schedule (HAS) and the Geriatric Mental State (GMS)-AGECAT. For the standardised degree of cognitive impairment Perneczky et al's MMSE criteria were applied. Mortality information was obtained from the official population registry. Multivariate Cox proportional hazard models were used to test the association between MMSE degrees of cognitive impairment and mortality risk. We also estimated the PAF of mortality due to specific MMSE stages.
Results.Cognitive impairment was associated with mortality risk, the risk increasing in parallel with the degree of cognitive impairment (Hazard ratio, HR: 1.18 in the ‘mild’ degree of impairment; HR: 1.29 in the ‘moderate’ degree; and HR: 2.08 in the ‘severe’ degree). The PAF of mortality due to severe cognitive impairment was 3.49%.
Conclusions.A gradient of increased mortality-risk associated with severity of cognitive impairment was observed. The results support the claim that routine assessment of cognitive function in older adults should be considered in clinical practice.
Contributors
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- By Lassi Alvesalo, Alberto Anta, Juan Luis Arsuaga, Shara E. Bailey, Priscilla Bayle, José María Bermúdez de Castro, Tracy K. Betsinger, Luca Bondioli, Scott E. Burnett, Concepcion de la Rúa, William N. Duncan, Ryan M. Durner, Heather J.H. Edgar, Scott M. Fitzpatrick, Michael R. Fong, Ana Gracia-Téllez, Theresa M. Grieco, Debbie Guatelli-Steinberg, Tsunehiko Hanihara, Brian E. Hemphill, Leslea J. Hlusko, Michael W. Holmes, Jean-Jacques Hublin, Toby E. Hughes, John P. Hunter, Joel D. Irish, Kent M. Johnson, Sri Kuswandari, Christine Lee, John R. Lukacs, Roberto Macchiarelli, Laura Martín-Francés, Ignacio Martínez, María Martinón-Torres, Arnaud Mazurier, Yuji Mizoguchi, Stephanie Moormann, Greg C. Nelson, Stephen D. Ousley, Oliver T. Rizk, G. Richard Scott, Roman Schomberg, Kes Schroer, Christopher M. Stojanowski, Grant C. Townsend, Christy G. Turner, Theresia C. Weston, Bernard Wood, Clément Zanolli, Linhu Zhang
- Edited by G. Richard Scott, University of Alaska, Fairbanks, Joel D. Irish, Liverpool John Moores University
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- Book:
- Anthropological Perspectives on Tooth Morphology
- Published online:
- 05 March 2013
- Print publication:
- 21 February 2013, pp viii-xi
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Optical and Structural Characterization of Li-doped CdS Nanoparticles
- U. Sandoval, M. E. Hernández Torres, J. M. Gracia Jimenez, N. R. Silva González
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- Journal:
- MRS Online Proceedings Library Archive / Volume 1509 / 2013
- Published online by Cambridge University Press:
- 23 April 2013, mrsf12-1509-cc03-37
- Print publication:
- 2013
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CdS:Li nanoparticles were grown by the thermolysis method using a surfactant to control the nanoparticles growth and the passivity of the dangling bonds. The effect of the Li incorporation on the optical and structural properties of the CdS nanoparticles was studied by means of the optical transmission, photoluminescence, X-ray diffraction and HR-SEM&TEM techniques. The optical energy band gap lies in the interval from 2.7 to 3.6 eV. The photoluminescence spectra present a band with peak at 465 nm, which is indicative of the quantum confinement. The energy peak position (465 nm) is blue-shifted respect to the bulk material (512 nm). Then, one can infer that the energy band gap and the peak intensity vary according to the nominal lithium concentration in the growth solution. An average crystallite size of about 5 nm was estimated by the Brus equation and the Debye-Scherrer formula, and confirm by HR-SEM&TEM measurements.
Cool and hot executive functions in medication-naive attention deficit hyperactivity disorder children
- B.-R. Yang, R. C. K. Chan, N. Gracia, X.-Y. Cao, X.-B. Zou, J. Jing, J.-N. Mai, J. Li, D. Shum
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- Journal:
- Psychological Medicine / Volume 41 / Issue 12 / December 2011
- Published online by Cambridge University Press:
- 01 June 2011, pp. 2593-2602
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Background
This study aimed to compare ‘cool’ [working memory (WM) and response inhibition] and ‘hot’ (delay aversion) executive functions (EFs) in children with and without attention deficit hyperactivity disorder (ADHD).
MethodA total of 100 ADHD children (45 with family history of ADHD and 55 with no family history) and 100 healthy controls, all medication free, were tested on tasks related to the ‘hot’ (i.e. two choice-delay tasks) and ‘cool’ domains of EF (i.e. Digits backward, Corsi Block Task backward, Go/No-Go Task, Stop-Signal Task, and the Stroop).
ResultsCompared with the controls, children with ADHD were found to perform significantly worse on one or more measures of response inhibition, WM, and delay aversion after controlling for co-morbidities and estimated IQ. In addition, comparisons between ADHD children with family history of ADHD and those with no family history found significant differences on measures of response inhibition and WM but not delay aversion. These results are largely supported by results of two logistic regressions.
ConclusionsADHD was found to be associated with deficits on both cool and hot EFs. There is also evidence to suggest that cool EFs impairment is related to a family history of ADHD. Findings of this study have helped to elucidate the nature and extent of EF deficits in children with ADHD.