It is argued that two large groups of disorders can be distinguished in the field of psychopathology, (1) which divide between them the psychoses, neuroses and personality disorders; ( 2) the dynamics of which are those of Klein's paranoid-schizoid and depressive positions, respectively; and (3) which are distinguished by nine basic contrasts in symptomatology and dynamics, all of which are expressive of the opposition self-centred/other-centred. These three hypotheses form the interpersonal model of psychopathology, and are supported by argument from works of Foulds, Jung, Abraham, Fairbairn, Klein, Angyal, Winnicott and Heidegger. It is suggested that the interpersonal model can facilitate the dialogue between psychoanalysis and phenomenology

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Parmi leurs applications prometteuses, les lignées de cellules souches embryonnaires humaines (hES) présentent un potentiel inestimable pour améliorer la compréhension des mécanismes moléculaires et cellulaires impliqués dans le développement de maladies monogéniques. Cette application de modélisation pathologique est devenue possible grâce à l’utilisation de lignées hES porteuses de la mutation causale d’une maladie monogénique, obtenues au cours d’un diagnostique pré-implantatoire. L’équipe dans laquelle j’ai effectué mes travaux de thèse a démontré que des lignées hES et leurs progénies, porteuses de la mutation causale de la dystrophie myotonique de type 1 (DM1), exprimaient des défauts moléculaires caractéristiques de la pathologie, permettant ainsi leur analyse de façon plus pertinente par rapport à des cultures primaires dérivées de biopsies de patients et validant l’utilisation de ce modèle cellulaire. Dans ce contexte, dans la première partie de mon travail de thèse, mon objectif a été de mettre au point des conditions de culture permettant la différenciation des cellules hES normales et mutantes vers le lignage neural afin d’obtenir des populations homogènes de progéniteurs neuraux et de cellules souches neurales, puis de les caractériser sur le plan phénotypique et fonctionnel. Par une étude transcriptomique, j’ai ensuite comparé le profil d’expression de ces progéniteurs neuraux à une autre population homogène de précurseurs mésenchymateux. J’ai ainsi identifié des gènes et des voies de signalisation spécifiques à chacune de ces populations. (Article 1). Dans la seconde partie de mes travaux, ma contribution au projet de modélisation pathologique de DM1 a été d’utiliser ces progéniteurs neuraux et les cellules souches neurales mutés pour explorer les mécanismes physiopathologiques responsables des symptômes neurologiques observés dans cette pathologie. J’ai ainsi identifié une anomalie dans une voie de signalisation cellulaire perturbée, la voie la voie mTORC1, basée sur l’observation selon laquelle les cellules NSC porteuses de la mutation DM1 proliféraient plus lentement que les cellules contrôles (Article II). J’ai également étudié l’expression la protéine Tau, connue pour son implication dans la maladie d’Alzheimer, et mis en évidence des modifications suggérant une altération du transport axonal dans les neurones issus des lignées hES mutantes. Ces résultats, associés à ceux réalisés dans l’équipe, permettent d’apporter la preuve de concept de l’intérêt d’un tel modèle cellulaire pour la modélisation pathologique des maladies monogéniques. / Among their promising applications, human embryonic stem cells lines (hES) have huge potential to improve the understanding of molecular and cellular mechanisms involved in the development of monogenic diseases. This application of modeling pathologic became possible using hES cell lines carrying the causal mutation of a monogenic disease, obtained during pre-implantation diagnosis. The team where I did my thesis work demonstrated that hES cell lines and their progeny, carrying the causal mutation in myotonic dystrophy type 1 (DM1), expressing the molecular defects characteristic of the pathology, allowing more relevant analysis than primary cultures derived from biopsies of patients and validates the use of this cell model. In this context, in the first part of my thesis, my goal was to develop culture conditions for hES cell differentiation into normal and mutant neural lineage in order to obtain homogeneous populations of neural progenitors and neural stem cells and to characterize their phenotypic and fonctional preperties. Next, using a transcriptomic method, I compared the expression profile of neural progenitors to another homogeneous population of mesenchymal precursors. Thus, I identified genes and signaling pathways specific to each of these populations. (Article 1). In the second part of my work, my contribution to the pathological modeling of DM1 was to use these mutant neural progenitor cells and neural stem cells to explore the pathophysiological mechanisms involved in neurological symptoms observed in this pathology. Thus, I have identified a cell signaling pathway defects in mTORC1 pathway based on the observation that NSC cells carrying DM1 mutation proliferated more slowly than control cells (Article II).At last, I also studied the expression of Tau protein, a protein involved in Alzheimer’s disease and I have highlighted changes suggesting impairement of axonal transport in neurons derived from hES cell lines mutant. These results, together with those performed in the team, can provide proof of concept for the benefit of such a cell model for modeling disease monogenic diseases.

Reward and punishment have been studied in the laboratory for their relative effects on learning processes and on perceptual processes they have been studied in the classroom for their relative effects on learning and on modification of performance of various motor and mental tasks; they have been studied in relation to intellectual, age and sex factors, and temperamental or personality factors; and they have recently been studied in a clinical setting in connection with problems of psychopathology, The studies concerned with personality variables reflect a broadening concern with personality dynamics that has accompanied the recent rapid expansion of interest in the clinical area of psychology. They strongly suggest that there are differences related to personality factors in the effects and perhaps the effectiveness of rewarding and punishing incentive conditions. It was to explore some of the implications of these studies and to extend the empirical data in this area that the present research was designed. It was to explore some of the implications of these studies and to extend the empirical data in this area that the present research was designed. To provide a framework for the discussion which follows the major aspects of two studies will be outlined. / This thesis was digitized as part of a project begun in 2014 to increase the number of Duke psychology theses available online. The digitization project was spearheaded by Ciara Healy.

M.A. (Clinical Psychology) / The theory on the interpretation of dreams is one of Freud's most important contributions to psychology. Unfortunately very little empirical research of Freudian dream theory has been done because of the difficulty in operationalizing Freudian concepts. In this study an attempt has been made to overcome this difficulty by introducing an empirical referent namely manifest dream content. The aim of this study is to indicate that there is a correspondence between personality types and manifest dream content ...

背景:人類的思維可以構思為一個由很多「結」(nodes) 互相連接而組成的認知網絡(cognitive network) 。這個認知網絡從兒時開始發展及建立。只有那些有較強聯繫關係的結才會一同起動，從而影響我們的反應。不同的心理病態相信有不同的認知網絡。本研究旨在探索不同的心理病患的認知網絡，包括焦慮、抑鬱及具攻擊性。 / 研究方法:是項研究分為兩個階段，數據分別從臨床病患及社區人士中收集。第一階段旨在使用自由聯想法(Free association technique) 探究不同組別對焦慮、抑鬱及其攻擊性的觀念。數據由三個個別組別，包括83 個抑鬱症病患、139 焦慮症病患、43 個具攻擊性人士，及相對的105 、102 和110 個社區人士中集得。收集到的短句、詞語或描述會被整理及排序。在第二階段中，資料從另外108、106及102個臨床病患和相對的114、102及101 個社區人士三個個別組別中收集。他們需要評估在第一個階段中制定的認知觀念量表。獲得的數據會透過SPSS 的多元尺度法(Multidimensional Scaling) 進行分析，從而了解不同的認知網絡。 / 結果:得到抑鬱、焦慮、及具攻擊性的三幅認知網絡的圖像。進一步的分析顯示抑鬱症患者的認知網絡傾向聯繫抑鬱反應，但卻較少聯繫到正面的應對方式。相反，對照組則較偏向把抑鬱和正面的應對方式聯繫在一起。焦慮、症患者較容易聯想到一些長期、不間斷的社會心理壓力，例如跟家庭有關的問題和工作。不過，對照組則傾向把焦慮、聯繫到一些偶發性的不利事情，例如交通意外和死亡。具攻擊性的人較常想及有關個人不公平的情況，例如低薪及長工作時間，但對照組較多聯想到不公平的社會狀況，例如商業社會。 / 結論:研究資料顯示抑鬱、焦慮和具攻擊性的認知網絡可以透過自由聯想法和多元尺度的分析方法識別出來。研究發現臨床病患跟社區成人在認知網絡上有不同的聯繫模式。是項研究的其中一個重要貢獻是制定了跟抑鬱、焦慮及具攻擊性三份認知觀念量表，可用作衡量及比較抑鬱、焦慮及具攻擊性的認知網絡的工具。 / Background: Our mind can be conceptualized as a cognitive network depicting as a string of inter-linked nodes which developed since childhood from daily experiences. Only nodes which share stronger association strengths are expected to co-activate to guide our reactions. Different cognitive networks are believed operating in different psychopathological states. This study sought to explore the cognitive networks of different psychopathology, namely, anxiety, depression, and aggression. / Method: The study composed of two stages and data was collected from clinical patients and community adults. The first stage aimed at construct generation (i.e., to explore the nodes) of depression, anxiety, and aggression using the technique of free association. Three separate groups of 83 depressed patients, 139 anxiety patients, and 43 aggressive individuals, and three corresponding community controls of 105, 102, and 110 were recruited. The obtained phrases, words, or descriptors were tabulated and rank ordered. In Phase 2, another three disordered groups of 108, 106, and 102 individuals and three corresponding community controls of 114, 102, and 101 were asked to rate on the construct lists generated in Phase 1. Multidimensional Scaling (MDS) analysis using SPSS was employed to empirically model the networks. / Results: Three separate visual maps of anxiety, depression, and aggression were obtained. Further analyses showed that depressed patients acquire a cognitive network involving mainly depressive responses. Yet, they are not so likely to activate positive coping in their cognitive network. On the other hand, normal controls tend to associate depression with positive coping. Anxiety patients more likely associate anxiety with psychosocial stressors like family and work which is considered to be unremitting whereas community controls more likely relate anxiety with adverse life events such as traffic accidents and death which are sporadic. Aggressive individuals more likely to think of unfairness relating to personal injustice and inequality such as low wages and long working hours while the normal controls more likely associate aggression with unfairness related to broad societal concerns and injustice such as commerce. / Conclusion: Findings show that cognitive networks of depression, anxiety, and aggression can be successfully identified by using the technique of free association and MDS. Clinical patients have different association patterns than the community controls. An important contribution of this study is to generate three construct lists which contain cognitive constructs on depression, anxiety, and aggression, and to evaluate and compare the cognitive networks of different psychopathology. Implications of the findings were discussed. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Wong, Mei Ting. / "December 2011." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2012. / Includes bibliographical references (leaves 178-200). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese; some appendixes also in Chinese. / ABSTRACT --- p.i / ACKNOWLEDGEMENTS --- p.v / TABLE OF CONTENTS --- p.ix / LIST OF TABLES --- p.xii / LIST OF FIGURES --- p.xiv / CHAPTER / Chapter I --- COGNITIVE MODEL OF PSYCHOPATHOLOGY --- p.1 / Introduction --- p.1 / The Cognitive Model --- p.3 / Schema-focused Therapy --- p.11 / Schema and Psychopathology --- p.13 / Origins and Development of Schemas --- p.19 / Schema Activation --- p.25 / Summary --- p.26 / Chapter II --- NETWORY THEORY OF AFFECT --- p.27 / Network Theory --- p.27 / Network Theory of Affect --- p.30 / Research Related to the Network Theory of Affect --- p.34 / Summary --- p.43 / Chapter III --- EXPECTANCY AND BEHAVIOR --- p.45 / Expectancy --- p.45 / Alcohol Expectancy Memory Network --- p.47 / Conclusion --- p.52 / Chapter IV --- RESEARCH QUESTIONS --- p.53 / Research Questions and Objectives --- p.56 / Chapter V --- METHODS --- p.61 / The Present Study --- p.62 / Design --- p.62 / Participants --- p.64 / Instruments --- p.66 / Data Analysis --- p.83 / Pilot Study --- p.85 / Chapter VI --- RESULTS --- p.86 / Descriptive Statistics --- p.86 / Psychometric Properties of the Assessment Instruments --- p.94 / Refinement of Constructs Lists Generated in Phase One --- p.99 / Demographic Variables --- p.114 / Multidimensional Scaling --- p.121 / Chances of Co-activation between ConstructslNodes --- p.132 / Comparisons between Clinical and Community Groups --- p.140 / Chapter VII --- DISCUSSION --- p.159 / CognitiveNetwork of Different Psychopathology --- p.160 / Differences in Cognitive Networks between Clinical and Community Groups Free Association --- p.172 / Limitation of the Study and Future Direction --- p.174 / REFERENCES --- p.178 / APPENDICES A --- p.201 / APPENDICES B --- p.207 / APPENDICES C --- p.208

Ces travaux visaient à établir un protocole permettant de différencier des cellules pluripotentes (embryonnaires ou induites) en kératinocytes capables de générer un épiderme pluristratifié in vitro et in vivo pour la thérapie cellulaire et la modélisation pathologique. Dans une 1ère partie, des cellules hES ont été utilisées pour être différenciées en culture en kératinocytes. Ces cellules ont été caractérisées par des approches de RT-PCR quantitative, FACS et d’immunofluorescence. De plus, leur potentiel immunogène a été évalué par l’analyse en FACS des protéines du CMH de classe I et II. La capacité de ces kératinocytes à reformer un épiderme stratifié a été démontrée in vitro,sur une matrice synthétique, mais aussi in vivo après greffe sur souris immunodéficientes. Dans une 2ème partie, des cellules hIPS ont ensuite été dérivées en kératinocytes avec le même protocole. Si la caractérisation des kératinocytes issus des hIPS a produit des résultats positifs, la possibilité de maintenir ces cellules en culture s’est révélée impossible dans les conditions utilisées. De même, alors que la stratégie visait à modéliser les épidermolyses bulleuses, l’interférence avec l’expression de protéines impliquées dans la jonction épidermo-dermique n’a pas été couronnée de succès. Par contre, des nouvelles hIPS mutées ont pu être générées puis différenciées en kératinocytes, prouvant ainsi la possibilité d’utiliser cette démarche pour modéliser la pathologie. Dans une 3ème partie, une étude d’expression différentielle a permis de démontrer que les kératinocytes dérivés des cellules pluripotentes surexpriment la kératine 19 (marqueur foetal) par rapport à des kératinocytes postnataux. / This work aimed to establish a protocol for the differention of pluripotent cells (embryonic or induced) into keratinocytes, which must be able to generate a pluristratified epidermis in vitro as well as in vivo for cell therapy and pathological modeling. In the 1st part of this work, a new protocol was developped to derive keratinocytes from hES cells. These cells were characterized by using RTq-PCR, FACS and immunofluorescence assays. Their immunogenicity was also evaluated by FACS analysis of class I and class II MHC proteins. The capacity of these keratinocytes to generate a pluristratified epidermis has been proved in vitro as well as in vivo following grafts onto immunodeficient mice. In a 2nd part of this work, hIPS cells were then derived into keratinocytes using the same protocol. The characterization of heratinocytes derived from hIPS produced positive results, but it was unfortunately not possible to maintain those cells in culture. Similarly, a strategy based on RNA interference against dermoepidermal junction proteins was not successful; but new hIPS mutated cell lines have been established and differentiated into keratinocytes, proving the feasibility of such an approach for pathological modeling. In a 3rd part of this work, a differential expression study proved that keratinocytes derived from pluripotent cells overexpress keratin 19 (marker fetus) when compared with postnatal keratinocytes.

La maladie de Huntington (MH) est une maladie neurodégénérative héréditaire. Elle est causée par l'expansion d'un motif CAG qui codant une séquence de poly-glutamine (polyQ) dans le gène huntingtine (HTT). La survenue des symptômes de la maladie est tardive. Pour étudier la MH, un grand nombre de modèles génétiques animaux et cellulaires ont été utilisés au cours des 15 dernières années sans se traduire en traitements bénéfiques de façon durable pour les patients. Les médicaments disponibles servent actuellement à gérer les symptômes de la maladie, et n’ont pas d’effet sur le pronostic létal. Les modèles existants semblent incapables de répliquer pleinement les premières anomalies transcriptionnelles intervenant dans la MH. J’ai tiré profit de la disponibilité de lignées de cellules hESC-MH et émis l'hypothèse qu’elles sont adaptées au déchiffrement des mécanismes pathologiques ou correcteurs impliqués dans la phase pré-symptomatique de la MH, du développement embryonnaire à la vie adulte. J'ai développé des protocoles et des outils cellulaires et moléculaires pour établir les hESC mutantes et normales comme modèle cellulaire de la MH. Puis j’ai utilisé ces cultures pour explorer par une approche transcriptomique la dérégulation transcriptionnelle dans les cellules neurales immatures porteuses de la mutation causale de la MH. J’ai identifié de nouveaux biomarqueurs cellulaires précoces associés à la mutation causale de la MH. Ces résultats suggèrent l’existence de mécanismes moléculaires encore inconnus et spécifiques des phases les plus précoces de la maladie. Ces découvertes pourraient fournir des cibles originales pour une intervention pharmacologique pré-symptomatique. / Huntington’s Disease (HD) is a neurodegenerative inherited disease. It is caused by the extension of a CAG motif coding for a poly-glutamine (polyQ) tract within huntingtin gene (HTT). Symptoms declaration occurs late in life. In order to better understand HD a wealth of cellular and animal genetic models both have fuelled 15 years of studies, but never transduced into truely lasting and beneficial pharmacological treatment. Avalaible drugs are used to handle symptomatology, but don’t address the lethal prognosis. Existing models seems to fail at replicating fully the first steps of transcriptionnal alterations occurring in HD. I took advantage of the recent disponibility of hESC naturally carrying HD mutation to investigate the hypothesis that they can yield insight into early presymptomatic mechanisms of HD from embryonic development to adulthood. I developed protocols, cellular and molecular tools to establish HD and normal hESC as HD cellular models. Then I used these tools to investigate transcriptomic dysregulation in immature neural cells carrying the HD causing mutation. I identified new early cellular biomarkers associated to the mutation. These results suggest the existence of previously unknown molecular mécanisms spécific to the earliest stages of the disease. These new biomarkers could be very interesting targets for pre-symptomatic pharmacological intervention.