Le neurofeedback est typiquement considéré par le monde médical comme une technique prometteuse dans le traitement du TDAH, mais dont l'efficacité spécifique n'est pas suffisamment bien établie. La présente étude cherche à déterminer des effets spécifiques au neurofeedback sur le fonctionnement intellectuel et sur les comportements d'enfants présentant un TDAH. Pour ce faire, deux expérimentations ont été réalisées auprès de 46 enfants au total (15 enfants lors de la première expérimentation et 31 pour la deuxième), âgés de 7 à 13 ans et ayant un diagnostic de TDAH (tous déjà traités avec une médication psychostimulante). L'entraînement de neurofeedback visait à augmenter l'amplitude du rythme sensori-moteur (12-15 Hz) et à diminuer l'amplitude des ondes Thêta (4-8 Hz) au-dessus du cortex sensori-moteur droit (C4). La première expérimentation impliquait des enfants recevant le neurofeedback et d'autres en liste d'attente. Elle visait d'abord à récolter les enregistrements EEG requis pour la condition placebo de l'étude suivante et à identifier les variables les plus susceptibles de montrer l'efficacité du traitement. Elle pouvait aussi déjà démontrer une certaine efficacité du protocole de neurofeedback choisi. En cela et malgré la prise en compte du grand nombre de variables examinées, deux sous-échelles « TDAH » du questionnaire CBCL complété par les parents ont montré des améliorations significatives pour les enfants ayant bénéficié du neurofeedback. Le questionnaire DuPaul rempli par les parents montrait aussi un effet crédible, mais en deçà du seuil statistique corrigé pour le grand nombre de variables examinées dans cette étude préliminaire. La deuxième expérimentation reprenait les mêmes conditions en ajoutant un groupe placebo avec double insu (concernant les groupes placebo et neurofeedback). Le but de la condition placebo était de déterminer que c'est bien la modulation de l'EEG et non la relation établie avec les parents du groupe entraîné qui amène les améliorations rapportées. Les enfants sélectionnés ont été répartis aléatoirement en trois groupes (vrai neurofeedback, neurofeedback placebo, attente). La tendance vers un effet significatif au DuPaul-parent de la première étude et la contribution de l'entraînement de l'EEG ont été confirmées à l'étude 2 puisque des améliorations significatives ont été observées pour le groupe d'enfants ayant bénéficié du vrai neurofeedback par rapport aux deux groupes contrôles sur deux des trois sous-échelles du questionnaire DuPaul-parent (« Inattention » et « Totale »). Toutefois, les améliorations significatives obtenues lors de la première expérimentation au CBCL n'ont pas été reproduites, ce qui demeure inexpliqué. Des gains aux échelles partielles « Compréhension verbale » et « Mémoire de travail » ainsi qu'à l'échelle globale de l'épreuve d'intelligence ont aussi été observés, ce qui n'avait pas été le cas lors de la première expérimentation. Notons toutefois que ces gains n'étaient pas suffisamment importants pour franchir le seuil de signification avec la correction de Bonferroni (p ≤ .01) spécifiée a priori. En conclusion, les résultats obtenus mettent en évidence des effets spécifiques au neurofeedback agissant notamment sur les symptômes comportementaux du TDAH. Rappelons que ces effets n'ont pas été observés pour le groupe en condition placebo. D'autres recherches sont nécessaires pour reproduire ces résultats et éventuellement, mieux comprendre le fonctionnement de ce traitement afin d'être en mesure de l'utiliser de façon optimale. ______________________________________________________________________________ MOTS-CLÉS DE L’AUTEUR : Neurofeedback, TDAH, enfants, placebo

Recently the question of eco-labelling has become increasingly important, especially when used as a green marketing tool. Surprisingly, the marketing placebo effect of eco-labelling and the influence it has on the performance of a product has received little attention. The purpose of this study is to explain the placebo effect of eco-labelling on consumer attitudes. Fishbein’s model of attitudes is implemented whereby a focus group is used as a basis to create a questionnaire and a tasting experiment. The findings of the study provide an explanation and evidence of the placebo effect of eco-labelling. The product with an environmental label is perceived as tastier, healthier and of higher quality than the same product without ecological label.

No description available.

Thesis (M.Tech.: Chiropractic)--Durban University of Technology, 2009 / Objective: The efficacy of manipulation as compared to placebo in the treatment of two groups of weight trainers with Acromioclavicular (AC) Joint Dysfunction. Methods: Twenty patients (n=20), using randomised sampling were allocated to two intervention groups. Patients in each group received four treatments each over a two-week period and assessed at initial, one week, two weeks and one month follow ups. Objective measures included Algometer and Inclinometer readings. Numerical Pain Rating Scales (NRS), Shoulder Rating Questionnaire (SRQ) and the Shoulder Pain and Disability Index (SPADI) measured subjective outcomes. Results: Manipulation demonstrated significant improvement in objective findings. Subjective outcomes did not show significant difference between the manipulation and placebo groups. Conclusion: Manipulation, when compared to placebo, can be considered as an effective treatment intervention for the treatment of AC joint dysfunction with particular reference to objective outcomes. Although, caution needs to be utilised in accepting this outcome due to limitations in sample size, subjective measure sensitivity and specificity as well as the stringency of the inclusion and exclusion criteria.

One of the most interesting aspects of human beings is their ability to choose a course of action and strive to achieve it. When participating in therapeutic interventions involving physical activities, people may allocate different amounts of effort, persistence and commitment to succeed in them. The reason for this difference lies in their motivation. The present thesis focuses on the energising of behaviour, that is, the differential effort and motivation that people put into therapeutic activities. Placebo responses are generally explained by the mechanisms of response expectancy, conditioning and motivational concordance. Findings presented in this thesis partially supported motivational concordance, testing for the first time that therapeutic outcome after engagement in intrinsically motivated tasks requiring physical activity was explained both by response expectancy and motivational concordance . The effects of response expectancy, perceptions of effort and intrinsic motivation on therapeutic benefit and mood change were investigated in both laboratory (Studies 1-4) and real-life therapeutic contexts (Study 5). Study 1 showed that effort mediated the effects of expectancy on perceived benefit, and effort predicted both positive and negative affect following the performance of a breathing exercise. Study 2 showed that differences in outcome between guided imagery and meditation were very small, but that non-specific factors play the major role in outcome. Study 3 showed that perceiving a task as difficult enhances effort perceptions, intrinsic motivation and therapeutic outcome. Motivated behaviour predicted therapeutic outcome but not expectancy. Study 4 showed that the provision of success feedback enhances outcome expectancies, motivated behaviour and mood change. Expectancies, motivation and effort predicted positive affect, whereas only effort predicted negative affect. Finally, results from Study 5 suggest that placebo responses may differ in real-life therapeutic interventions according to the strength motivational factors are elicited within the intervention. Both expectancy and motivated behaviour predicted change in positive affect, whereas motivated behaviour predicted change in negative affect and empowerment. Therapeutic outcome and its underlying mechanisms are likely to reflect a mixture of response expectancies and intervening motivational factors.

Heidelberg, Univ., Dipl.-Arb., 2006.

Diplomarbeit Hochschule für Angewandte Psychologie Zürich, 2007.

Made available in DSpace on 2013-08-07T19:04:36Z (GMT). No. of bitstreams: 1 000395365-Texto+Completo-0.pdf: 1650433 bytes, checksum: 314debda01604f166f617cfc3552807d (MD5) Previous issue date: 2005 / Background: The efficacy of sertraline hydrochloride to prevent intradialytic hypotension has not been established. Methods: A cross over double-blind, randomized, placebo-controlled study was performed with 18 patients presenting more than 15 hypotension episodes in the last 25 hemodialysis sessions. One group received eight weeks of sertraline hydrochloride 50mg/daily followed by eight weeks of placebo. The second group received eight weeks of placebo followed by eight weeks of sertraline hydrochloride 50mg/daily. Data from the four final weeks of each eight-week period were considered. The following variables were assessed: weight, ultrafiltration, arterial blood pressure, hypotension episodes, nursing interventions, laboratory data and depressive symptoms (Beck Inventory). Data were analyzed using the usual statistical methods and a model which identifies interference by a period (practice) or period-treatment (carry-over) effect. Results: At baseline, the mean number of hypotensive episodes per session was 0. 8 ± 0. 1 [median 0. 7 (0. 6 - 0. 9)], vs. 0. 5 ± 0. 4 [0. 33 (0. 08 - 0. 83)] with sertraline use and 0. 3 ± 0. 2 [0. 21 (0. 17 - 0. 42)] with placebo. The number of hypotensive episodes before the study was significantly higher than during placebo (p = 0. 001) and sertraline treatment (p = 0. 027). The number of hypotension episodes and nursing interventions was similar during placebo and sertraline use. A period-treatment effect was observed for the variables Beck depression score and successful ultrafiltration. A period effect was observed for pre- and post-dialysis weight and successful ultrafiltration. A treatment effect was observed for interdialytic gain and ultrafiltration that were higher in the placebo group, and for number of hypotensive episodes per session, that was lower in this group. Conclusion: Sertraline was not useful to prevent intradialytic hypotension in the present study. / Introdução: A eficácia do cloridrato de sertralina para prevenir Hipotensão Arterial Intradialítica (HID) não está estabelecida. Métodos: Foi realizado um estudo duplo cego cruzado, randomizado, controlado com placebo em 18 pacientes, que apresentaram mais de 15 episódios de hipotensão nas últimas 25 sessões de hemodiálise. Um grupo recebeu oito semanas de sertralina 50mg/dia seguido de oito semanas de placebo. Outro grupo recebeu placebo seguido de sertralina. Apenas os dados das quatro semanas finais de cada período foram considerados. As seguintes variáveis foram avaliadas: peso, ultrafiltração, pressão arterial, episódios de hipotensão, intervenções de enfermagem, dados laboratoriais e escore depressivo (Inventário de Depressão de Beck). Os dados foram analisados usando o método estatístico usual e modelo que identifica a interferência do efeito de período, e do efeito de interação entre período e tratamento. Resultados: Antes do estudo, o número de episódios de hipotensão por sessão foi de 0,8 ± 0,1 [mediana 0,7 (0,6 – 0,9], significativamente maior que 0,5 ± 0,4 [0,33 (0,08 – 0,83)] usando sertralina (p = 0,027) e que 0,3 ± 0,2 [0,21 (0,17 – 0,42)] usando placebo (p = 0,001). O número de episódios de hipotensão e de intervenções de enfermagem foi similar durante o período de uso de placebo ou sertralina. Efeito de interação entre período e tratamento foi observado para escore depressivo e sucesso de ultrafiltração. Efeito de período foi observado para as variáveis de peso pré e pós-diálise e sucesso de ultrafiltração. Efeito de tratamento foi observado para as variáveis de ganho de peso interdialítico e ultrafiltração, que foram maiores no grupo em uso de placebo e para número de episódios de hipotensão/sessão, que foi menor nesse grupo. Conclusões: O uso de sertralina não foi efetivo em prevenir os episódios de hipotensão intradialítica no presente estudo.

Glucocorticoid excess as a result of Cushing’s syndrome or pharmacological treatment can result in the development of obesity and type 2 diabetes mellitus (T2DM). The reactivation of cortisone to cortisol is catalysed by 11βHSD1 which is expressed widely but notably in adipose tissue and liver. Studies have shown dysregulation of cortisol in these tissues with obesity potentially promoting the development of T2DM. Inhibition of 11βHSD1 has been attempted as a novel treatment for T2DM with observed improvement in glycaemic control, body weight and blood pressure. The efficacy of such agents has been disappointing with few reaching phase 2 trials. With recent evidence of bidirectional activity of 11βHSD1 in vivo it becomes apparent that dysregulation may occur at an intracellular rather than tissue level. In this thesis I address several key outstanding questions concerning the physiology and regulation of 11βHSD1 including: 1. Whether combined therapy with metformin alters 11βHSD1 activity and obscures the efficacy of 11βHSD1inhibitors; 2. Whether the contribution of 11βHSD1 to local cortisol concentrations has been under-estimated by considering total rather than free cortisol turnover; and 3. Whether recycling between cortisol and cortisone in adipose tissue and skeletal muscle in obesity is a neglected feature of 11βHSD1 biochemistry and function. Eight obese healthy men with and without type 2 diabetes were recruited to a randomised placebo controlled cross over trial. They received 4 weeks treatment with metformin and placebo. Participants with T2DM additionally received gliclazide as a further control. Using the deuterated tracer D4-cortisol 11βHSD1 activity was measured. Metformin treatment increased whole body 11βHSD1 in both groups postulated as a result of improved insulin sensitivity. 11βHSD1 is located within cells and so contributes to free tissue cortisol concentrations but perhaps less so to total (protein-bound) cortisol in plasma. It has been shown that 11βHSD1 contributes almost half of total circulating cortisol concentrations at rest. This measurement relied upon blood sampling during steady state deuterated cortisol (D4-cortisol) infusion with measurements of total (free plus protein bound) cortisol which may have underestimated true 11βHSD1 activity. This was therefore investigated by comparing 11βHSD1 activity as calculated using total compared with free cortisol tracer enrichments. Equilibrium dialysis was performed separating free from bound portions in plasma samples taken from healthy volunteers who received D4-cortisol infusion. Analysis revealed similar measurements of 11βHSD1 activity using free compared with total cortisol implicating rapid turnover of glucocorticoids between the free and bound pools. On first discovery 11βHSD1 was seen to be a dehydrogenase enzyme in vitro. Later work recognised reductase activity in vivo and up until recently 11βHSD1 has been viewed as a predominantly reductase enzyme. As with other enzymes in the same family, the ability to catalyse both reductase and dehydrogenase depends upon the availability of substrate and co substrate. Whether dysregulation of 11βHSD1 in the settings of obesity and T2DM is the result of alteration in directionality at a cellular level is not known. Firstly bidirectional activity of 11βHSD1 was confirmed in vitro using HEK-293 cells stably transfected with 11βHSD1. The influence of obesity and acute perturbation with hyperinsulinaemia was subsequently investigated in vivo in a random order cross over single blinded case control study involving ten normal weight and ten obese healthy male volunteers. D4-cortisol and deuterated cortisone (D2-cortisone) were infused for the measurement of reductase and dehydrogenase activity of 11βHSD1 respectively with measurements taken across forearm muscle and abdominal subcutaneous adipose tissue. Across whole body, lean and obese individuals displayed similar 11β-reductase and 11β-dehydrogenase activity. Across tissue, 11β-reductase and 11β-dehydrogenase activity was different from zero across adipose tissue in obese individuals and across skeletal muscle in lean individuals providing further evidence of tissue specific differences in 11βHSD1 with obesity. With the addition of hyperinsulinaemia, reductase and dehydrogenase activity was somewhat increased in lean individuals although there was no statistically significant difference between lean and obese individuals. Across tissue there was a trend for obese individuals to display increased 11β-reductase activity across adipose tissue with hyperinsulinaemia. Comparing the rates of reductase and dehydrogenase activity revealed predominantly reductase activity across tissue in obese and dehydrogenase activity in lean individuals. The development of direction specific inhibitors targeting reductase activity by 11βHSD1 may prove efficacious for the treatment of obesity. In conclusion, 11βHSD1 acts as a bidirectional enzyme in vitro and in vivo. Overall directionality of enzyme activity is altered in a tissue specific manner in the setting of obesity. We have shown that this intracellular regulation of cortisol is reflected equally in the metabolically active free pool and total plasma pool. The efficacy of 11βHSD1 inhibitors as novel agents for the treatment of T2DM and coexisting obesity is not diminished by co-prescription with metformin but may prove more efficacious through the development of reductase specific inhibitors.

Submitted by Diogo Misoguti (diogo.misoguti@gmail.com) on 2016-06-15T12:34:21Z No. of bitstreams: 1 Publico-capa.pdf: 1364190 bytes, checksum: 2a60b84b83c88eafef204f40d1549ac5 (MD5) / Approved for entry into archive by Diogo Misoguti (diogo.misoguti@gmail.com) on 2016-06-15T12:35:40Z (GMT) No. of bitstreams: 1 Publico-capa.pdf: 1364190 bytes, checksum: 2a60b84b83c88eafef204f40d1549ac5 (MD5) / Made available in DSpace on 2016-06-15T12:35:40Z (GMT). No. of bitstreams: 1 Publico-capa.pdf: 1364190 bytes, checksum: 2a60b84b83c88eafef204f40d1549ac5 (MD5) Previous issue date: 2006 / Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) / Objetivo: O objetivo deste estudo foi comparar o efeito do tratamento hormonal do hormônio Gonadotrofina Coriônica Humana (HCG), em dois esquemas posológicos diferentes, ao placebo quanto sua efetividade e segurança no tratamento da Criptorquidia. Métodos: Este estudo é um ensaio clínico randomizado, duplo-cego, placebo-controlado de 14 semanas. A amostra de 92 pacientes que foram randomizados para o grupo-HCG dias alternados, denominados de Grupo G1 (N = 29), para o grupo HCG a cada quatro dias, denominados Grupo G4 (N= 33) e o grupo-placebo, denominados como Grupo O(N = 30). 2. Os desfechos clínicos primários para este estudo foram 1) Cura, 2) Melhora, 3) Não Cura. Os desfechos complementares foram: 4) Efeitos adversos, 5) Níveis séricos hormonais. Resultados: Não existiram diferenças entre os grupos HCG dias alternados, HCG a cada quatro dias e placebo para as medidas dos desfechos primários. 1) Cura: G1: 3/29(3,3%), G4: 4/33(4,3%) e O: 3/30(3,3%) 2) Melhora: G1:3/29(3,3%), G4: 1/33(1,1%) e O: 3/30(3,3%). 3) Não Cura: G1: 23/29(25%), G4: 28/33(30,4%) e O: 24/30(26,1%) p=0,815. 4) Os efeitos adversos mais freqüentes em nossa amostra foram: Aumento do numero de ereções: não foi possível avaliar. 5) Níveis séricos hormonais: Testosterona sérica: G1: de 34,15 ± 5,8ng/ml; G4: 49,6± 5,6 ng/ml e O: 7,5± 3,5ng/ml. Hormônio Luteinizante (LH): G1: 0,22± 0,2 , G4: 0,07±0,1 e O: 0,08±0,02 Hormônio Folículo Estimulante (FSH): G1: 0,88±0,16, G4: 0,3±0,1 e O 1,15±0,6. Conclusão: Não foi encontrada nenhuma diferença estatística no tratamento com HCG, independente da posologia adotada, e placebo. Os autores concluem a hormonioterapia com HCG não demonstrou superioridade na eficácia e ou segurança no tratamento da criptorquidia ao placebo. / Objective: The objective of this study is to compare the effect of hormone treatment with Human Chorionic Gonadotropin (HCG) with two different posological schemes compared to placebo treatment regarding its effectiveness and safety in the treatment of cryptorchidism. Methods: This study is a 14-day double-blind, placebo-controlled, randomized clinic assay. Ninety two patients were randomized into a group-HCG alternate days, identified as G1 Group (N=29); a group HCG every other four days, identified as G4 Group (N=33); and a placebo group, identified as Group O (N = 30). The primary clinical findings of this study were: 1) Cure, 2) Improvement, 3) Uncured. The complementary findings were: 4) Adverse effects, 5) Hormone serum levels. Results: There were no differences between the HCG alternate days, hCG every other 4 days, and the placebo groups for the primary findings. 1) Cure: G1: 3/29(3.3%), G4: 4/33(4.3%) and O: 3/30(3.3%) 2) Improvement: G1:3/29(3.3%), G4: 1/33(1.1%) and O: 3/30(3.3%). 3) Uncured: G1: 23/29(25%), G4: 28/33(30.4%) and O: 24/30(26.1%) p=0.815. 4). The most frequent adverse effects in our sample were: increase in the number of erections: impossible to assess. 5) Hormone serum levels: Serum testosterone: G1: 34.15 ± 5.8ng/ml; G4: 49.6± 5.6 ng/ml and O: 7.5± 3.5ng/ml. Luteinizing Hormone (LH): G1: 0.22± 0.2, G4: 0.07±0.1 and O: 0.08±0.02. Follicle-Stimulating Hormone (FSH): G1: 0.88±0.16, G4: 0.3±0.1 and O 1.15±0.6. Conclusion: No differences were found in the treatment with HCG independently of the posology employed and placebo. The authors concluded that hormone therapy with HCG was not effective in cryptorchidism treatment in relation to placebo.