Stigma is one of the key barriers to mental health services and there has been growing efforts to develop anti-stigma programs. However, little research has been done on quantifying experiences of stigma and their psychosocial impacts in the perspectives of those that suffer from mental illnesses. It is essential to develop an instrument that quantifies the extent and impact of stigma. Therefore, we conducted a study to field-test The Inventory of Stigmatizing Experiences and measure the difference in perceived stigma and its psychosocial impacts on Korean and Canadian patients with Depression and Bipolar disorders. A cross-sectional comparison study was conducted. Data collection took place at tertiary care hospitals located in Kingston, Ontario, Canada and Seoul, South Korea. In total, 214 Canadian and 51 Korean individuals with depression and bipolar disorder participated. Canadian participants reported significantly higher experience with stigma (p << 0.05) and its impact (p << 0.05) compared to Korean participants. Moreover, patients with bipolar disorder had significantly higher scores on both stigma experience and impact compared to patients with depression (p << 0.05). However, the diagnosis status was not a significant factor in the linear regression analyses, whereas nationality remained as a strong predictor of stigma. Age of symptom onset was also a strong predictor for both stigma experience and stigma impact. Marital status was also a significant factor for stigma impact. Both subscales of the inventory (the stigma experiences scale and the stigma impact scale) were highly reliable, with reliability coefficients of 0.81 and 0.93, respectively. In conclusion, there seems to be higher level of stigma and impact in the Canadian population compared to the Korean population. In addition, bipolar disorder patients may experience more stigma and higher impact compared to patients with depression. These differences in stigma experience and its impact in different populations (by nationality and diagnosis) suggest the need to develop more tailored anti-stigma programs. The Inventory of Stigmatizing Experiences is a highly reliable instrument. / Thesis (Master, Neuroscience Studies) -- Queen's University, 2012-08-17 12:23:14.762

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Numerous studies have demonstrated the impact of organic cation (OCTs; SLC22 family) and anion transporters (OATs; SLC22 family) on the efficacy and safety of clinically important therapeutics. To be specific, OCTs and OATs have been identified as determinants for uptake into and secretion from enterocytes, hepatocytes and renal proximal tubular cells, and are frequent sites of drug-drug interaction (DDI). In addition, OCTs expressed in brain are components of the low-affinity, high capacity clearance pathway (uptake-2) for biogenic monoamine neurotransmitters. As a result, OCTs may represent novel targets for mood disorders. The inhibitory effects of several therapeutic agents, designed drugs and novel compounds were assessed on the function of OCTs/Octs and OATs/Oats. Among these compounds, the anthraquinone rhein showed significant inhibition on hOATs. While the antituberculosis drug ethambutol, the herbal products matrine and oxymatrine, synthetic cathinones, and all quinazoline and guanidine compounds produced significant inhibition on hOCT activity with most IC50 values in the micro- and even nanomolar ranges. Considering the clinically relevant unbound concentrations in biofluids, significant DDI potentials were found for rhein, ethambutol, matrine, oxymatrine and several synthetic cathinones affecting enterocytes, hepatocytes and/or proximal tubules. As hOCT2 and hOCT3 may participate in modulating neurotransmitter homeostasis in the CNS, these findings also suggested that the CNS pharmacological effects of synthetic cathinones, quinazoline and guanidine compounds might be due to their inhibitory effects on OCTs; although their impact may be limited solely to clearance of these compounds. Based upon their in vitro OCT/Oct inhibition profiles, three lead quinazoline and guanidine compounds were chosen for in vivo studies. Potent antidepressant-like effects of one lead hOCT-interacting compound (KEO-099) were re-confirmed in the tail suspension test. While in vivo results of the two newly identified hOCT-interacting lead compounds were somewhat less clear. Finally, homology modeling and docking studies for hOCT3 identified key amino acid residues that might be involved in interaction between hOCT3 and small molecules. Subsequent experiments confirmed a competitive mode of interaction between MPP+ and lead compounds on hOCT3. Thus, preliminary analysis indicates our hOCT3 homology model can be used to support rational drug design and high-throughput screening of novel hOCT substrates/inhibitors.

This study is an investigation into the psychosocial themes present in the DSM-IV diagnosis of adolescents diagnosed with a comorbid Disruptive Behavior and Mood Disorder. These themes are viewed from a psychosocial theoretical perspective. The study focuses on answering four questions. Firstly, what are the psychosocial themes present in the diagnosis of adolescents diagnosed with a comorbid Disruptive Behavior and Mood Disorder? Secondly, how does these themes impact the adolescents psychosocial development? · Thirdly, what role does these themes play as causative factors of Disruptive Behavior and Mood Disorder symptoms in adolescence? · and lastly does these themes represent interactional processes reinforcing a reciprocal pattern of behavior and mood disorder symptoms? These questions are all viewed taking the psychosocial development of the adolescent into account. / Dissertation (MA (Clinical Psychology))--University of Pretoria, 2005. / Psychology / unrestricted

La dépression est fréquente, sa prise en charge difficile et les connaissances de sa physiopathologie très incomplètes. Il est établi qu’il existe une composante familiale et héréditaire au trouble dépressif mais le substrat biologique de cette vulnérabilité est inconnu et souvent les études souffrent d’un manque de reproductibilité. Par ailleurs, il n’existe pas de bio-marqueur validé utilisable en pratique courante.Nous proposons dans ce travail de thèse d’explorer les ARN périphériques chez les patients souffrant de dépression de façon à explorer s’ils peuvent définir des bio-marqueurs et si leur étude peut nous permettre de mieux comprendre le processus physiopathologique.Nous avons recruté des patients souffrant de dépression sévère dans plusieurs études pour répondre à nos objectifs. Nous avons été attentif dans ces études à des problèmes méthodologiques importants, en particulier à propos du choix des gènes de contrôle pour les PCR en temps réel, du choix de critères statistiques dans l’étude pan-génomique et de la prise en compte de prélèvements répétés chez les sujets sains pour contrôler toute variation due à des facteurs non contrôlés. En accord avec une abondante littérature sur le sujet, nous avons pu mettre en évidence des gènes déjà décrits dont l’expression transcriptionnelle est dérégulée chez les patients par rapport aux sujets contrôles ou au cours de l’évolution de la dépression, dans des études centrées sur des gènes candidats et une étude pan-génomique.Nous avons pu également mettre en évidence de façon nouvelle l’expression dérégulée chez les patients déprimés de gènes impliqués dans la régulation chromatinienne ou l’expression des gènes.Nous avons également pu nous rendre compte que les approches pan-génomiques complétaient l’approche gène candidat avec une meilleure convergence que ne le laissait supposer la littérature.Nous avons également étudié les micro-ARN et mis en évidence qu’un certain nombre d’entre eux étaient des marqueurs traits ou des marqueurs liés à l’état au cours de la dépression.L’ensemble des données issues de notre étude pan-génomique et de notre étude sur les micro-ARN montre qu’il existe des interactions probables entre les micro-ARN et les ARNm dérégulés et ces données confirment le rôle possible des gènes régulant la chromatine ou l’expression des gènes dans la dépression.Enfin, l’étude des variabilités inter- et intra-individuelles de l’expression génétique confirme l’absence d’altération globale de la transcription au cours de la dépression et souligne l’importance d’un ensemble de molécules régulant la transcription dont l’expression est contrainte c’est à dire très peu variable d’un individu à l’autre et d’un moment à l’autre chez un même sujet.Si nous n’avons pas pu mener une étude validant des marqueurs biologiques, nos résultats ouvrent la voie à l’exploration à plus grande échelle de ces marqueurs potentiels comme à l’étude d’hypothèses originales sur la physiopathologie de la dépression. / Major depression is a frequent and severe disease whose treatment is often inconsistent and patients care remains insufficient. Despite some hypothesis which implicate mono-amine and genetic factors, the pathophysiology of major depression remains unclear. Moreover, no biological marker is available in current clinical practice.Our work aims to propose methodological tools and offers preliminary results to develop such biological markers by studying gene expression in peripheral blood mononuclear cells from severe depressive patients and sex and age-matched controls in different comparative prospective studies. Candidate gene and pangenomic approaches were combined. Moreover, we explored for the first time human microRNA transcription variation in major depression by multiplex RT-qPCR.Among our main findings, we demonstrate that some well-known candidate gene such as serotonin transporter mRNA could be interesting biomarkers of major depression evolution or prognosis. In addition, pangenomic study highlights the implication of genes related to chromatin structure and gene expression regulation like histone family. We also identified variations in the expression of a set of microRNAs during a major depressive episode and, with in silico approaches, we propose putative functional interactions between candidate miRNAs and mRNAs.Overall, our work underlines the feasibility and the relevance of studying the level of expression of RNAs in a psychiatric disorder using peripheral tissues. We obtained both convergent and novel results in regard to previous investigations opening the way to better knowledge of major depression pathophysiology as well as biomarkers development.

OBJETIVOS: Avaliar associações prospectivas dos transtornos de humor e da religiosidade com o risco de suicídio em adultos jovens provenientes da população geral. MÉTODO: Coorte prospectiva de base populacional. Adultos jovens (18-24 anos) foram recrutados e acompanhados em média cinco anos depois. Risco de suicídio, transtornos de humor e de ansiedade foram avaliados usando o Mini-International Neuropsychiatric Interview. Transtornos por uso de substâncias foram avaliados utilizando o Alcohol, Smoking and Substance Involvement Screening Test. A religiosidade foi avaliada na linha de base e agrupada de acordo com a afiliação religiosa e de acordo com a freqüência de participação. RESULTADOS: A amostra incluiu 1560 adultos jovens na linha de base, com 1244 reavaliados no seguimento (80,6%). Os episódios depressivos, tanto atuais como prévios, tiveram um impacto significativo no risco de suicídio. Os episódios maníacos prévios, no entanto, foram associados com uma menor consistência a um risco de suicídio. Nenhuma associação da religiosidade com o risco de suicídio foi encontrada nas duas etapas da pesquisa. Este resultado permaneceu na análise em todas as afiliações religiosas, mesmo quando subdivididas de acordo com a freqüência de participação. CONCLUSÕES: Os episódios depressivos têm um robusto efeito prospectivo, independente, sobre o risco de suicídio. O efeito dos episódios maníacos, por outro lado, foi dependente da análise e merece uma melhor investigação. Embora existam evidências prévias sugerindo um papel protetor da religiosidade sobre o risco de suicídio, essas não foram confirmadas nessa amostra específica de adultos jovens. / OBJECTIVES: To assess the prospective associations of mood disorders, religiosity and suicidality in a community sample of young adults. METHODS: Prospective population-based cohort study. Young adults (18-24 years old) were recruited and followed-up five years later. Suicidality, mood and anxiety disorders were assessed using the Mini-International Neuropsychiatric Interview. Substance use disorders were assessed using the Alcohol, Smoking and Substance Involvement Screening Test. Religiosity were assessed at baseline and grouped according to religious affiliation and according to attendance frequency. RESULTS: The sample included 1560 young adults at baseline, with 1244 reassessed at follow-up (80.6%). Depressive episodes, both current and past had a significant impact on suicidality. Previous manic episodes, however, were less consistently associated with suicidality. No association of religiosity with suicidality was found in the two waves of the research. This effect is maintained in all religious affiliations, even when subdivided the analysis according to the frequency of attendance in religious service. CONCLUSIONS: Depressive episodes have an independent and robust effect on prospective suicidality. The effect of manic episodes, on the other hand, was dependent on the analysis and deserves further exploration. Although there is prior general evidence suggesting a protective role of religiosity on suicidality, these were not confirmed in this specific sample of young adults.

Prior to the 1990s, bipolar disorder, a behavioral disorder characterized by severe mood fluctuations, was not considered an suitable diagnosis for children. However, in recent decades, an increase in pediatric bipolar disorder (PBD) diagnosis has occurred in the U.S. The purpose of this study was to explore the perceptions and lived experiences of licensed mental health clinicians regarding their decision-making processes used during assessment and diagnosis of PBD. This phenomenographic study utilized individual, semi-structured interviews to explore the perceptions and lived experiences of 14 licensed clinicians in the Commonwealth of Massachusetts who assess and diagnose PBD. Data were collected with a 7-question face to face interview. Using NVivo 10 software several key phrases and words were identified, coded, and used to locate patterns, themes, and concepts. Data analysis revealed that significant issues related to PBD assessment and diagnosis may exist, including: inconsistencies in assessment/diagnostic processes; reticence to diagnose the disorder; failure to use available assessment instruments; a lack of attention to comorbidities; and trouble differentiating between PBD symptoms and other issues, such as trauma or dysfunctional family dynamics. Given the reluctance of these mental health professionals to diagnose PBD, implications for social change underscore the important role of education, training, and ongoing clinical supervision to help other mental health professionals accurately assess and diagnose PBD. Recommendations emanating from study findings suggest further research on PBD assessment and diagnosis to help professionals develop more effective diagnostic frameworks for clinical training and practice.

Background. General population data were used to study co-morbidities between lifetime social phobia and mood disorders. Methods. Data come from the US National Comorbidity Survey (NCS). Results. Strong associations exist between lifetime social phobia and major depressive disorder (odds ratio 2·9), dysthymia (2·7) and bipolar disorder (5·9). Odds ratios increase in magnitude with number of social fears. Reported age of onset is earlier for social phobia than mood disorders in the vast majority of co-morbid cases. Temporally-primary social phobia predicts subsequent onset of mood disorders, with population attributable risk proportions of 10–15%. Social phobia is also associated with severity and persistence of co-morbid mood disorders. Conclusions. Social phobia is a commonly occurring, chronic and seriously impairing disorder that is seldom treated unless it occurs in conjunction with another co-morbid condition. The adverse consequences of social phobia include increased risk of onset, severity and course of subsequent mood disorders. Early outreach and treatment of primary social phobia might not only reduce the prevalence of this disorder itself, but also the subsequent onset of mood disorders.

Fetma och psykisk ohälsa är två utbredda folkhälsoproblem som förutom att orsaka stor samsjuklighet, även ger stora ekonomiska förluster för samhällena. Den här systematiska litteraturstudien gjordes i syftet att undersöka eventuell förekomst av sambandet mellan fetma och psykisk ohälsa. I denna studie avses psykisk ohälsa som ångest, låg sinnesstämning och depression. Pub Med och Lib Hub användes för datainsamling. Vid urval av artiklarna var en av de huvudsakliga etiska principerna att artiklarna måste blivit granskade. Efter urval analyserades och jämfördes den insamlade data. Det resultat som framkom var inte helt entydigt, det står klart att samband finns men de är av olika karaktär. Ett starkare samband har hittats hos kvinnor, lågutbildade och personer med fetma (BMI på &gt;35), det finns även skillnader inom olika etniciteter. Vidare forskning föreslås vara av mer världsomfattande och långsiktig karaktär, med entydig mätmetod, för att göra resultatet mer generaliserbart och användbart vid interventioner i en rad av kontexter. / Obesity and mental illness are two global public health problems which causes not only comorbidity but also huge economic losses for societies. This systematic review was carried out with the purpose to investigate the occurrence of the association between obesity and mental illness. In this study mental illness includes anxiety, low mood and depression. Databases that were used were Lib Hub and PubMed. Ethical criteria were met and the used articles had been peer reviewed. Collected data were then analyzed and compared. The results showed that there is an association between obesity and mental illness, although there are some differences. A stronger association is found in women, in the lower educated, in people with more severe obesity and for some ethnic groups. Further research proposed to be more global and made with the same measurement techniques, to make sure that the results are generalizable and usable in different contexts.

Bipolar disorder is a psychiatric illness characterized by recurrent fluctuations in mood and increased risk of suicide. Twin and family studies have identified the highly heritable nature of the disorder, but the limitations of the current DNA-centric paradigm underscore the need for a new perspective to gain a clearer understanding of its basis. This project investigates various facets of bipolar disorder from an epigenetic standpoint. We used mass spectrometry-based mapping of individual DNA modification differences of the brain-derived neurotrophic factor gene. Moreover, the epigenetic basis of suicidal behaviour in bipolar disorder was investigated using DNA methylation microarrays. We also used a newly-developed enrichment technique, mTAG, to interrogate chromosome-wide DNA modification profiles using tiling microarrays in post-mortem brains of bipolar disease patients and controls. Findings from these experiments highlight observable features of epigenomes of patients affected with mood disorders, and may further the understanding of the molecular origin of psychiatric diseases.