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1.
Educ Health (Abingdon) ; 24(3): 577, 2011 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-22267353

RESUMO

INTRODUCTION: DISCERN is an instrument designed to help patients assess the reliability of written information on treatment choices. Originally created in English, there is no validated Spanish version of this instrument. This study seeks to validate the Spanish translation of the DISCERN instrument used as a primary measure on a multicenter study aimed to assess the reliability of web-based information on treatment choices for attention deficit/hyperactivity disorder (ADHD). METHODS: We used a modified version of a method for validating translated instruments in which the original source-language version is formally compared with the back-translated source-language version. Each item was ranked in terms of comparability of language, similarity of interpretability, and degree of understandability. Responses used Likert scales ranging from 1 to 7, where 1 indicates the best interpretability, language and understandability, and 7 indicates the worst. Assessments were performed by 20 raters fluent in the source language. RESULTS: The Spanish translation of DISCERN, based on ratings of comparability, interpretability and degree of understandability (mean score (SD): 1.8 (1.1), 1.4 (0.9) and 1.6 (1.1), respectively), was considered extremely comparable. All items received a score of less than three, therefore no further revision of the translation was needed. CONCLUSION: The validation process showed that the quality of DISCERN translation was high, validating the comparable language of the tool translated on assessing written information on treatment choices for ADHD.


Assuntos
Transtorno do Deficit de Atenção com Hiperatividade/tratamento farmacológico , Padrões de Prática Médica/estatística & dados numéricos , Redação , Comunicação , Tomada de Decisões , Humanos , Internet , Idioma , Reprodutibilidade dos Testes
2.
Br J Pharmacol ; 160(3): 772-83, 2010 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-20590579

RESUMO

BACKGROUND AND PURPOSE: Methamphetamine (METH) is a psychostimulant amphetamine that causes long-term dopaminergic neurotoxicity in mice. Hypodopaminergic states have been demonstrated to increase voluntary ethanol (EtOH) consumption and preference. In addition, the endocannabinoid system has been demonstrated to modulate EtOH drinking behaviour. Thus, we investigated EtOH consumption in METH-lesioned animals and the role of cannabinoid (CB) signalling in this EtOH drinking. EXPERIMENTAL APPROACH: Mice were treated with a neurotoxic regimen of METH, and 7 days later exposed to increasing concentrations of drinking solutions of EtOH (3, 6, 10 and 20%). Seven days after neurotoxic METH, the following biochemical determinations were carried out in limbic forebrain: CB(1) receptor density and stimulated activity, 2-arachidonoyl glycerol (2-AG) and monoacylglycerol lipase (MAGL) activity, dopamine levels and dopamine transporter density. KEY RESULTS: EtOH consumption and preference were increased in METH-treated mice. Seven days after METH, a time at which both dopamine levels and density of dopamine transporters in limbic forebrain were decreased, CB(1) receptor density and activity were unaltered, but 2-AG levels were increased. At this same time-point, MAGL activity was reduced. The CB(1) receptor antagonist AM251 prevented the METH-induced increase in EtOH consumption and preference, while N-arachidonoyl maleimide, an inhibitor of MAGL, increased EtOH consumption and preference in both saline- and METH-treated mice. CONCLUSIONS AND IMPLICATIONS: An increase in endocannabinoid tone may be involved in the increased consumption of and preference for EtOH displayed by METH-lesioned mice as blockade of the CB(1) receptor decreased EtOH-seeking behaviours, whereas the MAGL inhibitor increased EtOH consumption.


Assuntos
Consumo de Bebidas Alcoólicas/fisiopatologia , Consumo de Bebidas Alcoólicas/psicologia , Ácidos Araquidônicos/fisiologia , Estimulantes do Sistema Nervoso Central/toxicidade , Glicerídeos/fisiologia , Metanfetamina/toxicidade , Síndromes Neurotóxicas/psicologia , Consumo de Bebidas Alcoólicas/metabolismo , Amidoidrolases/metabolismo , Animais , Ácidos Araquidônicos/metabolismo , Comportamento de Escolha/efeitos dos fármacos , Comportamento de Escolha/fisiologia , Dopamina/metabolismo , Proteínas da Membrana Plasmática de Transporte de Dopamina/metabolismo , Endocanabinoides , Glicerídeos/metabolismo , Sistema Límbico/efeitos dos fármacos , Sistema Límbico/metabolismo , Sistema Límbico/patologia , Sistema Límbico/fisiologia , Masculino , Metanfetamina/antagonistas & inibidores , Camundongos , Camundongos Endogâmicos C57BL , Monoacilglicerol Lipases/antagonistas & inibidores , Monoacilglicerol Lipases/metabolismo , Síndromes Neurotóxicas/metabolismo , Piperidinas/farmacologia , Alcamidas Poli-Insaturadas/metabolismo , Pirazóis/farmacologia , Receptor CB1 de Canabinoide/metabolismo , Receptor CB1 de Canabinoide/fisiologia
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