Dissertations / Theses on the topic 'Models of disorder'

Thesis (Ph. D.)--University of Kentucky, 2008.
Title from document title page (viewed on October 30, 2008). Document formatted into pages; contains: vi, 43 p. Includes abstract and vita. Includes bibliographical references (p. 33-39).

Epilepsy accounts for 0.5% of the global burden of disease, and primary prevention of epilepsy represents one of the three 2007 NINDS Epilepsy Research Benchmarks. Efforts to understand and intervene in the process of epileptogenesis have yielded fruitful preventative strategies in animal models. This article reviews the current understanding of epileptogenesis, introduces the concept of a "critical period" for epileptogenesis, and examines strategies for epilepsy prevention in animal models of both acquired and genetic epilepsies. As proof of principle, we investigated whether early preventative treatment during epileptogenesis in the WAG/Rij rat model of primary generalized epilepsy would persistently suppress the epilepsy phenotype in adulthood. Oral ethosuximide was given from age p21 to 5 months, covering the established period for epileptogenesis in this model. We then assessed the epilepsy phenotype by performing electroencephpalogram (EEG) recordings at serial time points after treatment cessation and by immunocytochemically measuring the cortical expression of ion channels Nav1.1, Nav1.6, and HCN1, which are dysregulated in epileptic WAG/Rij rats. Treatment both persistently suppressed seizures, even up to 3 months after treatment cessation, and blocked ion channel dysregulation. These findings indicated that treatment during epileptogenesis prevented the development of the epileptic phenotype. Subsequently, we investigated the C3H/HeJ mouse model of genetic epilepsy as a candidate for future studies in preventative treatment during epileptogenesis. Serial EEG recordings were performed from p5 to 3 months of age. We found that C3H/HeJ mice underwent three distinct, stereotyped phases of seizure development, which suggests that this model would be an appropriate candidate for future research on prevention of epileptogenesis.

Thesis (Ph. D.)--University of Oregon, 2000.
Typescript. Includes vita and abstract. Includes bibliographical references (leaves 199-204). Also available for download via the World Wide Web; free to UO users.

Nel corso degli ultimi decenni la fisica sperimentale ha raggiunto notevoli traguardi nel campo della manipolazione di sistemi di atomi freddi, riaccendendo l'interesse della ricerca su sistemi a lungo studiati teoricamente, ma fino a poco tempo fa impossibili da realizzare sperimentalmente. Questa riaccesa attenzione ha permesso di sfruttare le moderne capacità di calcolo per studiare sistemi quantistici che ancora risultano di difficile realizzazione. In questo contesto si inserisce il rinnovato interesse per i sistemi quantistici monodimensionali caratterizzati dalla presenza di potenziale disordinato. Questi presentano proprietà di trasporto particolari e sotto particolari condizioni sono oggetto di una transizione di localizzazione. La maggior parte degli studi in questo campo rivolgono la loro attenzione a sistemi di particelle fermioniche interagenti. In questo lavoro di tesi analizziamo, invece, sistemi quantistici fermionici non interagenti, mettendo in luce quanto già noto e proponendo strumenti di analisi derivati dallo studio dei sistemi interagenti. In particolare, proponiamo un'analisi statistica dei livelli energetici e poniamo le basi per futuri studi a riguardo.

Holographic dualities are now an established tool in the study of universal properties of strongly coupled field theories. Yet, theories without translational symmetry are still poorly understood in this context. In this dissertation, we investigate three new approaches to this challenging problem. The first part of the dissertation concerns a class of phenomenological holographic models in which momentum relaxation can be achieved without breaking translational symmetry in the dual geometry. In particular, we focus on an example in which the dual geometry is similar to anti-de Sitter (AdS) Brans-Dicke theory. We study the thermodynamic and transport properties of the model and show that for strong momentum relaxation and low temperatures the model has insulator-like behaviour. In the second part, we go beyond the effective description and consider holographic theories which explicitly break translational symmetry. From the perspective of gravity, these theories translate to geometries that vary explicitly in the boundary space-like coordinates. We refer to these geometries as 'inhomogeneous' and investigate two approaches to study them. The first is motivated by the question: "what happens to a homogeneous geometry when coupled with a field varying randomly in space?". Starting from an AdS geometry at zero or finite temperature, we show that a spatially varying random Maxwell potential drives the dual field theory to a non-trivial infra-red fixed point characterised by an emerging scale invariance. Thermodynamic and transport properties of this disordered ground state are also discussed. The second is motivated by the complementary question: "how does a random geometry affect a probe field?". In the weak disorder limit, we show that disorder induces an additional power-law decay in the dual correlation functions. For certain choices of geometry profile, this contribution becomes dominant in the infra-red, indicating the breaking of perturbation theory and the possible existence of a phase transition induced by disorder. The third and last part of this dissertation switches from the gravity to the field theoretical side of the duality. We discuss the Sachdev-Ye-Kitaev (SYK) model, a disordered many-body model with distinctive black hole-like properties. We provide analytical and numerical evidence that these holographic properties are robust against a natural one-body deformation for a finite range of parameters. Outside this interval, this system undergoes a chaotic-integrable transition.

The microbiota-gut-brain axis is a multidirectional communication chain between the central and enteric nervous systems that relates brain function to peripheral intestinal functions. Gut microbiome composition is influential within the axis because different bacteria produce different shortchain fatty acid markers. Short-chain fatty acids can cross the blood-brain barrier to induce neuroinflammation and likely affect neural development. Autism spectrum disorder (ASD) is a neurodevelopmental disorder that has no defined etiology, cure, or therapeutic treatment. Neuroinflammation, microbiome alterations, and social deficits have been demonstrated in ASD. It is tempting to speculate that neuroinflammation caused by peripheral inflammation or microbiome products can induce abnormal brain development that results in social behavior deficits. However, to contribute to the previous statement a suitable animal model must be used. The current study uses three popular animal models that demonstrate social behavior deficits to determine if short-chain fatty acid profiles are different between the two models as well as a wild-type control strain. Fecal samples were collected from the following mouse strains between 90 and 120 days of development: C57BL/6J control mice, BTBR genetic knockout mice, C57BL/6J injected with valproic acid, and C57BL/6J injected with polycytidylic acid. The last two models were pregnant dams injected during day 11 of gestation. Short-chain fatty acid profiles were obtained from fecal samples to determine differences between the models. Percentages were obtained for the following short-chain fatty acids: acetic, propionic, isobutyric, butyric, isovaleric, and valeric acids. With this research, developmental cues that attribute to autism spectrum disorders may be better understood and, in the future, new preventative treatments may be advanced.

Muscle Dysmorphia (MD) has recently been conceptualized as the male form of Eating Disorders (ED), although it is not currently classified as an ED. The current study compares etiological models of MD symptomatology (based on Grieve's [2007] conceptual model of MD) and ED symptomatology (based on Stice's [1994] conceptual model of Bulimia Nervosa). In both models, it was hypothesized that sociocultural influences on appearance (SIA) would predict body dissatisfaction (BD), and that this relationship would be mediated by self-esteem (SE) and perfectionism (P); that BD would predict negative affect (NA); and that NA would predict MD and ED symptomatology. Two-hundred-forty-seven female and 101 male college students at a mid-south university completed the study via on-line data collection. All participants completed the Sociocultural Attitudes Toward Appearance Questionnaire-3, the State Self-Esteem Scale, the Multidimensional Perfectionism Scale, the Positive and Negative Affect Scale, The Eating Attitudes Test-26, and the Muscle Dysmorphic Disorder Inventory. Women completed the Body Shape Questionnaire, and men completed the Male Body Attitudes Scale. Multiple regression analyses were conducted to test each model's fit. In both models, most predictor paths were significant. However, in the MD model, SIA and P combined did not predict BD. The combined effects of SIA, SE, P, and BD failed to predict NA in both models. In the MD model, the combined effects of SIA, SE, P, BD, and NA failed to predict MD symptomatology. These results suggest that ED symptomatology and MD symptomatology etiological models are somewhat similar. It is suggested that P and NA be removed from future etiological models of MD.

New insights have revealed the complex and heterogeneous nature of reward-related behaviours: not only are different aspects of reward (e.g. reward 'liking' and 'wanting') subserved by dissociable neural mechanisms, but they are differentially expressed across major psychiatric disorders. The aim of this thesis was to investigate discreet reward-related processes, pertaining to the hedonic and cognitive processing of rewards, in relation to schizophrenia and depression preclinical models. The Methylazoxymethanol acetate (MAM) neurodevelopmental model of schizophrenia and the Wistar Kyoto (WKY) inbred depression model were chosen based on their good face and construct validities to the clinical conditions. Microstructural analysis of licking in simple drinking and contrast situations were used to investigate the constructs of consummatory and anticipatory anhedonia in these models. Whilst MAM-treated rats showed no behaviours indicative of consummatory or anticipatory anhedonia, WKY rats showed generally lower consummatory and palatability responses to sweet solutions and failed to suppress their palatability responses to a contrasted solution (when a preferred solution was expected). Therefore, WKY rats demonstrated behaviours analogous to deficits in both consummatory and anticipatory aspects of hedonic processing. To investigate cognitive processing of rewards, outcome devaluation and differential outcome paradigms were adopted, but no impairments on either task were found for the MAM model. In contrast, WKY rats were insensitive to post-conditioning changes in reward value and did not benefit from stimulus-correlated outcomes during the acquisition of a conditional discrimination task. Therefore, WKY rats do not appear to use the nature and /or value of rewards to guide their behaviours in the same manner as controls. In short, MAM-treated animals did not display the hedonic deficits or impaired instrumental behaviours expected for a comprehensive schizophrenia model. In contrast, the WKY inbred rat strain appears to be suitable in investigating manifestations of clinical depression in respect to reward-processing deficits.

Thesis (Ph. D.)--York University, 1998. Graduate Programme in Psychology.
Typescript. Includes bibliographical references (leaves 188-213). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://wwwlib.umi.com/cr/yorku/fullcit?pNQ39312.

This study investigated the use of "naturalistic stressors" such as physical restraint and animal pheromones on the etiology of Posttraumatic Stress Disorder in a murine model. Pilot data suggest that stress effects may lead to an increase in the amount of time needed for cutaneous wounds to heal. Pilot data to support the creation of this model are presented suggesting that a delayed stress response may inhibit healing rates. In the present study an animal model of PTSD was used to investigate the effect of stress on the immune system. Yehuda and Antelman's (1993) nonhuman animal model of Posttraumatic Stress Disorder was tested with respect to the animals' immune response to cutaneous wounding. Additionally, effects of stress on exploratory behavior and activity were examined. The findings support the hypothesis that restraint and pheremonal stress and housing arrangements influence the ability of mice to heal a 1.5 mm punch biopsy, and exploratory behavior. The findings also support a profile for the Post-Traumatic Mouse.
Ph. D.

Taphonomy is the study of the fate of information in the fossil record. Information can be lost through the partial or complete destruction of fossils, or through the disruption of their original spatial relationships. Information can be "gained" if the alteration of fossils allows environmental information to be retrieved. In Bahia la Choya, northern Gulf of California, bioerosion, dissolution/maceration, and abrasion produce distinctive textures on the surfaces of shells in intertidal and shallow subtidal environments. Shells from different environments possess different surface textures, suggesting that textures on fossil shells could serve as paleoenvironmental indicators. Algal bioerosion is the chief mode of shell alteration and destruction in Bahia la Choya, though dissolution/maceration and abrasion are locally important. Algal bioerosion of shell surfaces is accelerated by the grazing activity of snails, and is most intense where snails are abundant. Microstratigraphic resolution is limited by vertical mixing of fossils and by the reworking of older fossils into younger deposits. Stratigraphic disorder is the departure from perfect chronological order of fossils in a stratigraphic sequence. I simulated mixing and reworking of fossils by simple computer models, and measured stratigraphic disorder using rank correlation statistics. As modeled, mixing produces disorder slowly, and its effects can be minimized by increasing sample size at each horizon and by increasing the vertical spacing between sampled horizons (though this reduces vertical resolution). Reworking generates disorder more efficiently, and its effects are not reduced by increasing sample size or spacing. The generation of stratigraphic disorder in fossiliferous sediments can also be modeled using M (depth of vertical mixing), I (thickness of sedimentary increments), and L (taphonomic loss rate) as parameters. Increasing M increases the disorder generated, and increasing I and L decreases disorder. For a worst case--high M and low I and L--the vertical spacing between samples must at least 3 times M to ensure a 5% temporal overlap between adjacent samples. A 1% temporal overlap requires a vertical spacing of 4.6 times M.

In disordered alloys, atoms belonging to the same chemical element will exhibit different environments. This leads to variations in the atoms’ local electronic structures, which in turn leads to variations in the binding energies of their core levels. These binding energies can be measured experimentally using core level X-ray photoelectron spectroscopy (XPS). Therefore, in theory at least, core level XPS can be used to resolve different environments in alloys. However, to make this a reality one must understand how an atom’s local electronic structure, and hence the binding energies of its core levels, are affected by local environment. In this thesis, two simple phenomenological models are explored which purport to correctly describe the local electronic structure of disordered alloys. The first model which we consider has its roots in chemical intuition; specifically, the notion that pairs of unlike atoms, i.e. atoms belonging to different chemical elements, transfer a certain quantity of charge, while like atoms do not. Using this model - known as the optimised linear charge model (OLCM) - the relationship between an atom’s local electronic structure, core level binding energies, and its environment is explored in detail, both in the bulk of disordered alloys and near their surfaces. As well as ‘homogeneous’ disordered alloys, in which the concentrations of the alloy’s constituent elements are the same throughout the entire alloy, various ‘inhomogeneous’ disordered alloy systems are considered. These include alloys exhibiting surface segregation - in which the concentrations at the surface differ from those in the bulk - as well as interfaces between two metals with various levels of intermixing. The results of our investigation of bulk inhomogeneous alloys are compared to analogous ab initio results, which confirms the model’s viability as a tool for rationalising the relationship between local electronic structure, core level binding energies, and environment. More generally, our results also reveal a number of interesting new phenomena. Firstly, the widths of spectra in inhomogeneous disordered alloys are significantly larger in some cases than is possible in any analogous homogeneous disordered alloy. Secondly, differences between the concentrations of each element at the surface and deep within the bulk cause a shift in the work function of the alloy under consideration. The latter results in qualitatively different trends than one would expect if this phenomenon was ignored, and prompts an alternative interpretation of the results of a recent experimental study. The second model which we consider is a particular case of the charge-excess functional model, in which the realised charges on all atoms are those which minimise a particular expression for the total energy of the system, and whose accuracy has been well established. The underlying assumptions and properties of this model are explored in detail, adding insight into the nature of the screening and inter-atomic interactions in disordered alloys. The model is shown to be equivalent to the OLCM for the case of binary alloys, and can therefore be considered to be the generalisation of the OLCM for alloys containing more than two chemical elements. The model is also used to derive analytical expressions for various physical quantities for any alloy, including the width of core level XPS spectra and the Madelung energy. These expressions are then used to investigate how the physical quantities to which they pertain vary with the concentrations of each element in a homogeneous disordered alloy consisting of three elements. Among other things, it was observed that the width of the core level XPS spectra is maximised when the concentrations of the two elements in the alloy with the largest electronegativity difference have equal concentrations, while the remaining element has a vanishing concentration.

Thesis (Ph. D.)--University of Alabama at Birmingham, 2007.
Additional advisors: Richard Brown, Ioulia Karpechina, Ryoichi Kawai, Boris Kunin. Description based on contents viewed Feb. 5, 2008; title from title screen. Includes bibliographical references (p. 73-75).

Aquest doctorat. El projecte cobreix les investigacions sobre aïllants topològics (TI) de la família Bi2Se3 amb diferents defectes i l'estudi d'efectes de proximitat de TI a la heteroestructura de grafè amb TI. La primera part d'aquest projecte se centra principalment en l'efecte del desordre en les propietats electròniques de TI amb gruix ultrafí (<3 nm). S’ha trobat que la manca de coincidència de rotació entre capes quíntuples de TI pot augmentar el “gap” de volum dels TI però preservar la textura d'espín tipus Rashba en l'estat de la superfície; mentre que la hidrogenació en una superfície de TI pot ajudar a reduir l'efecte túnel quàntic i tancar el “gap” de superfície en el punt Γ amb la textura d'espín tipus Rashba per a la pel·lícula TI ultrafina. A més, aquest esquema també pot crear un altre punt Dirac (DP) en el punt M amb textura de spin tipus Dresselhaus. La segona part del projecte investiga els efectes de proximitat de TI dins de la heteroestructura de grafè / TI i el DP en el grafè es plega des del punt K / K 'a Γ punt de la zona Brillouin, a causa del plegament de la banda, trobant que l'alineació entre el substrat de TI i el grafè té un paper clau en la formació de l'estructura de la banda i la textura d'espín del grafè. La configuració d'apilament "hollow" podria induir la distorsió d'unió de Kekulé a la capa de grafè, donant com a resultat l'engrandiment del “gap” (3.2 meV) i el Rashba SOC, el que dóna com a resultat la precessió d'espín propera al Γ punt . A més, aquesta textura atípica de Rashba espín fa que la component d'espín fora del pla disminueixi gradualment a mesura que el punt k s'allunya del punt Γ, el que porta a la anisotropia de gir a la capa de grafè. D'altra banda, la configuració d'apilament "bridge" o "top" podria portar l'evident divisió de la banda en direcció lateral, que podria ser l'origen de l'efecte Edelstein en la capa de grafè; no obstant, no hi ha una anisotropia d'espín evident en aquesta configuració. Totes les primeres dues parts s’han dut a terme a través del càlcul de teoria funcional de la densitat (DFT) i s’ha construït un model d'unió ajustada (TB) per als resultats de DFT per tal de proporcionar una explicació analítica de l'estructura de la banda i la textura de l'spin de grafè en el dispositiu de heteroestructura. L'última part d'aquest doctorat. L'activitat de recerca se centra en estudiar l'efecte d'impureses magnètiques i no magnètiques amb un esquema de dopatge aleatori sobre les propietats electròniques dels TI. El càlcul numèric basat en el model 3D Fu-Kane-Mele TB mostra que el dopatge no magnètic en la superfície de TI només pot induir el potencial in situ a la superfície DP i elevar-lo cap amunt, preservant la textura estàndard d'espín tipus Rashba; paral·lelament, el dopatge magnètic podria trencar la simetria d'inversió de temps i obrir el “gap” de superfície amb l'anisotropia d'espín també, el que significa que la component d'espín fora del pla en la superfície TI dopada magnèticament disminueix gradualment a mesura que el punt k s'allunya del Γ punt. Els treballs de recerca en aquest projecte podrien proporcionar una guia per a la llista d'experiments sobre les propietats electròniques de TI amb diferents tipus de defectes i impureses (magnètics i no magnètics); particularment, l'estudi dels efectes de proximitat en els TI podrien explicar el fenomen fonamental bàsic observat en aquest dispositiu per a l'estudi de la dinàmica d'espín en el laboratori.
Este doctorado. El proyecto cubre las investigaciones sobre aislantes topológicos (TI) de la familia Bi2Se3 con diferentes defectos y el estudio de efectos de proximidad de TI en la heteroestructura de grafeno con TI. La primera parte de este proyecto se centra principalmente en el efecto del desorden en las propiedades electrónicas de TI con espesor ultrafino (<3 nm). Se ha encontrado que la falta de coincidencia de rotación entre capas quíntuples de TI puede aumentar el “gap” de volumen de los TI pero preservar la textura de espín tipo Rashba en el estado de la superficie; mientras que la hidrogenación en una superficie de TI puede ayudar a reducir el efecto túnel cuántico y cerrar el “gap” de los estados de superficie en el punto Γ con la textura de espín tipo Rashba para la película TI ultrafina. Además, este esquema también puede crear otro punto Dirac (DP) en el punto M con textura de espín tipo Dresselhaus. La segunda parte del proyecto investiga los efectos de proximidad de TI dentro de la heteroestructura de grafeno/TI y el DP en el grafeno se pliega desde el punto K / K' a Γ punto en la zona Brillouin, debido al plegamiento de la banda, encontrando que la alineación entre el sustrato de TI y el grafeno desempeña un papel clave en la formación de la estructura de la banda y la textura de espín del grafeno. La configuración de apilamiento “hollow” podría inducir la distorsión de unión de Kekulé a la capa de grafeno, dando como resultado el agrandamiento del “gap” (3.2 meV) y el Rashba SOC, lo que da como resultado la precesión de espín cercana al Γ punto. Además, esta textura atípica de Rashba espín hace que la componente de espín fuera del plano disminuya gradualmente a medida que el punto k se aleja del punto Γ, lo que lleva a la anisotropía de giro en la capa de grafeno. Por otro lado, la configuración de apilamiento “bridge” o “top” podría traer la evidente división de la banda en dirección lateral, que podría ser el origen del efecto Edelstein en la capa de grafeno; sin embargo, no hay una anisotropía de espín evidente en dicha configuración. Todas las primeras dos partes se han llevado a cabo a través del cálculo de la teoría funcional de la densidad (DFT) y se ha construido un modelo de unión ajustada (TB) para los resultados de DFT con el fin de proporcionar una explicación analítica de la estructura de la banda y la textura del spin de grafeno en el dispositivo de heteroestructura. La última parte de este doctorado. La actividad de investigación se centra en estudiar el efecto de impurezas magnéticas y no magnéticas con un esquema de dopaje aleatorio sobre las propiedades electrónicas de los TI. El cálculo numérico basado en el modelo 3D Fu-Kane-Mele TB mostró que el dopaje no magnético en la superficie de TI solo podía inducir el potencial in situ en la superficie DP y elevarlo hacia arriba, preservando la textura estándar de espín tipo Rashba; mientras, el dopaje magnético podría romper la simetría de inversión de tiempo y abrir el “gap” de superficie con la anisotropía de espín también, lo que significa que la componente de espín fuera del plano en la superficie TI dopada magnéticamente disminuye gradualmente a medida que el punto k se aleja del Γ punto. Los trabajos de investigación en este proyecto podrían proporcionar una guía para la lista de experimentos sobre las propiedades electrónicas de TI con diferentes tipos de defectos e impurezas (magnéticos y no magnéticos); particularmente, el estudio de los efectos de proximidad en los TI podrían explicar el fenómeno fundamental básico observado en dicho dispositivo para el estudio de la dinámica de espín en el laboratorio.
This PhD. project covers the researches on the Bi2Se3-family topological insulators (TIs) with different defects and the study of the proximity effects of TI in the heterostructure of graphene with TI. The first part of this project mainly focuses on the effect of disorder on the electronic properties of TI with ultrathin thickness (< 3 nm). It was found that rotation mismatch between quintuple of TI can enlarge the bulk gap of TI but preserve the Rashba type spin texture on the surface state; while, the hydrogenation on one TI surface can help reduce the quantum tunneling effect and close the surface gap at Γ point with Rashba type spin texture for ultrathin TI film. Furthermore, this scheme can also create another Dirac point (DP) at M point with Dresselhaus type spin texture. The second part of the project investigates in the proximity effects of TI within the heterostructure of graphene/TI and the DP on graphene is folded from K/K' point to Γ point in Brillouin zone, due to the band folding, and it was found that the alignment between TI substrate and graphene played the key role in forming the band structure and the spin texture of graphene. Hollow configuration could induce the Kekulé bonding distortion to graphene layer, mainly resulting in the enlarged gap (3.2 meV), and the Rashba SOC, resulting in the spin precession close to the Γ point. Furthermore, this atypcial Rashba spin texture has the out-of-plane spin component decrease gradually as the k point moves away from the Γ point, leading to the spin anisotropy on graphene layer. While, the bridge or the top configuration could bring the evident band splitting in lateral direction, which could be the origin of the Edelstein effect in graphene layer; however, there is no evident spin anisotropy in such configuration. All the first two parts were carried out through density functional theory (DFT) calculation and a tight binding (TB) model was built up and fitted to the DFT results in order to provide an analytical explanation for the band structure and the spin texture of graphene in the heterostructure device. The last part of this PhD. research work was to study the effect of both non-magnetic and magnetic impurities with random doping scheme on the electronic properties of TI. Numerical calculation based on 3D Fu-Kane-Mele TB model showed that non-magnetic doping on TI surface could only induce the onsite potential on the surface state and lift the DP upwards, preserving the standard Rashba type spin texture; while, the magnetic doping could break the time reversal symmetry and open up the surface gap with the spin anisotropy as well, which means the out-of-plane spin component on magnetically doped TI surface decreases gradually as the k point moves away from the Γ point. Research works in this project could provide a guideline to the experimentlist on the electronic properties of TI with different kinds of defects and impurities (magnetic and non-magnetic ones); particularly, the study of the proximity effect of TI could explain the basic fundamental phenomenon observed in such device for spin dynamics study in the laboratory.

The development of the central nervous system is dysregulated in neurodevelopmental disorders such as intellectual disability, autism spectrum disorder, and epilepsy. These three disorders have different clinical features, yet there is high comorbidity between them. They can be difficult to study due to their highly complex aetiologies, however there are various monogenic diseases that can cause all of them, including SYNGAP1 haploinsufficiency where the synaptic guanosine triphosphatase (GTPase)-activating protein (SYNGAP) protein levels are highly reduced; Fragile X syndrome where the fragile X mental retardation protein (FMRP) is no longer translated; and DNM1 epileptic encephalopathy where mutations in the Dynamin1 gene alter the protein function. These monogenic conditions are synaptopathies as the proteins affected play important roles in synapse stability and neurotransmission. Because of the high comorbidity between these disorders, it is hypothesised that there may be a common mechanism underlying them. We hypothesise that a deficit in presynaptic vesicle recycling may be part of a common mechanism underlying intellectual disability, autism spectrum disorder, and epilepsy especially in SYNGAP1 haploinsufficiency, Fragile X syndrome, and DNM1 epileptic encephalopathy. Using various fluorescent presynaptic activity reporters including synaptic pHluorins, tetramethylrhodamine dextran and calcium dyes to compare presynaptic activity in in vitro models of these monogenic conditions, we found differences in synaptic vesicle (SV) endocytosis in the genetically altered conditions compared to wildtype controls. We observed various SV endocytosis defects in clathrin-mediated endocytosis (CME) or activity-dependent bulk endocytosis (ADBE) in our models. We observed enhanced CME in SynGAP1 KO mouse hippocampal neurons. This enhanced SV endocytosis was accompanied by decreased SV cargo on the plasma membrane. Rat SynGAP1 KO hippocampal neurons did not display enhanced SV endocytosis, nor did neurons with the GTPase-activating (GAP) domain of SynGAP deleted. This was perhaps due to the altered time course of development between these rodent species. In mouse and rat models of Fragile X syndrome, CME was not altered compared to wildtype controls. However, in a rat model, we observed fewer nerve terminals undergoing ADBE which is the dominant SV endocytosis mode during elevated neuronal activity. De novo epileptic encephalopathy-associated mutations in DNM1 had differential effects on SV recycling through both CME and ADBE. Mouse hippocampal neurons overexpressing Dyn1R237W, Dyn1I289F and Dyn1H396D all showed less CME compared to overexpression of Dyn1WT. Moreover, fewer nerve terminals overexpressing Dyn1H396D were found to undergo ADBE. We also found that a large-conductance potassium (BK) channel opener can accelerate clathrin-mediated endocytosis and thus may be able to rescue the impaired SV endocytosis caused by these mutants. Although there is not yet a common underlying pathway at the presynaptic level between these conditions, SV recycling dysfunction is present across all of these models. Furthermore, we propose an axis of pathophysiology model where optimal SV endocytosis is required for optimised neural performance. We propose that either decreased or increased SV endocytosis can lead to the synaptic dysfunction observed in these models.

Thesis (M. Phil.)--Hong Kong University of Science and Technology, 2002.
Includes bibliographical references (leaves 58-59). Also available in electronic version. Access restricted to campus users.

Thesis (Ph. D.)--University of Oregon, 2002.
Typescript. Includes vita and abstract. Includes bibliographical references (leaves 223-225). Also available for download via the World Wide Web; free to University of Oregon users.

Efforts to objectively inform cannabis discourses include research on the epidemiology of cannabis abuse and dependence disorders or, collectively, cannabis use disorder (CUD). For my dissertation I identified classes of individuals based on intraindividual CUD trajectory patterns and contrasted trajectory classes with respect to clinical characteristics of CUD, developmental risk factors, and psychosocial outcomes. Identifying differences between trajectory classes provides evidence for the validity of trajectory-based CUD constructs and informs the development of comprehensive models of CUD epidemiology and trajectory-specific intervention approaches. My dissertation used data from the Oregon Adolescent Depression Project, a prospective epidemiological study of the psychiatric and psychosocial functioning of a representative community-based sample randomly selected from nine high schools across western Oregon. Four waves of data collection occurred between mid-adolescence and early adulthood and included diagnostic interviews and self-report questionnaires. Onset and offset ages of all CUD episodes were recorded. The reference sample included 816 participants who completed all diagnostic interviews. A series of latent class growth models revealed three distinct CUD trajectory classes through age 30: (1) a persistent increasing risk class; (2) a maturing out class, marked by increasing risk through age 20 and then a decreasing risk through early adulthood; and (3) a stable low risk class. Rates of cannabis dependence were similar across the persistent increasing and the maturing out classes. Trajectory classes characterized by a history of CUD were associated with a variety of childhood risk factors and measures of psychosocial functioning during early adulthood. Participants who were male, had externalizing disorders, and had psychotic experiences during early adulthood discriminated between the persistent increasing and the maturing out classes. Future research based on more diverse samples is indicated, as are well-controlled tests of associations between risk factors, trajectory class membership, and psychosocial outcomes. A better understanding of these relationships will inform etiological theories of CUD and the development of effective intervention programs that target problematic cannabis use at specific developmental stages. Designing targeted versus undifferentiated interventions for those at greatest risk for adult psychosocial impairment could be a cost-effective way to mitigate the consequences of CUD.

Thesis (M.A.)--Southern Illinois University Carbondale, 2008.
"Department of Psychology." Keywords: Eating disorders, Path analysis, South Asia, Women. Includes bibliographical references (p. 127-144). Also available online.

The implicit models of mental disorder held by a group of older adults (n=25) and younger adults (n=28) were examined, using a questionnaire focusing on vignette - case descriptions developed on the basis of previous research in the field. Older and younger adults were found to have highly comparable beliefs and opinions. There were some significant differences between the groups such as in the weight attached to certain causative factors in relation to specific problems and in terms of overall style of causal explanation, where older adults lay greater weight on the role of 'difficulties in personal relationships'. Older adults were also more likely to view inpatient psychiatric treatment as necessary for a number of problems and cited different sources for their views and opinions from younger adults. Clinical implications are discussed and suggestions for further research made.

In the present study, the author tested the validity of certain variables and paths from a model of eating disorder (ED) symptomatology (T. L. Tylka & L. M. Subich, 2004) along with several alternative models (i.e., including poor interoceptive awareness, ethnic identity, and body mass) within a sample of U.S. University women of South Asian origin. The original sample included 440 women, but responses differed based on graduate and international status. Therefore, path analytic procedures focused on 255 undergraduate, non-international women. Results indicated excellent fit for 5 models and adequate fit for the 6th model. Exploratory analyses did not support self-esteem as a moderator but did support the role of internalization of beauty standards in the ED symptomatology of South Asian American women (c.f., Reddy & Crowther, 2007). The results are discussed in light of their contributions, implications, and limitations.

O Transtorno da Depressão Maior (MDD) é uma doença muito difundida em todo mundo e com uma alta prevalência, principalmente em mulheres. Transtornos de humor são recorrentes e ameaçam a vida, devido ao risco de suicídio. Apesar disso, a etiologia do MDD ainda é pouco entendida e diversas hipóteses foram desenvolvidas na tentativa de explicá-la. Uma delas está ligada ao estresse. Distúrbios no eixo hipotálamo-hipófiseadrenal (HPA) estão presentes em cerca 70% de pacientes com depressão. Ao buscar um melhor modelo animal para estudo do impacto do estresse no desenvolvimento da depressão, chegamos ao estresse leve crônico (CMS). Em estudos prévios desenvolvidos neste laboratório, observamos que há diferenças entre tipos de estressores e os mediadores secretados na resposta do eixo HPA, isto é, durante o estresse físico é secretado o mediador vasopressina, enquanto que no estresse psicológico, é secretado o mediador CRF; já nos estresses considerados mistos (como nado forçado), ambos os mediadores estão presentes. Assim, propusemos estabelecer protocolos de CMS baseados no protocolo original de Paul Willner, pesquisador que desenvolveu este modelo, empregando estressores do tipo físico ou psicológico, separadamente. O que observamos foi que nenhum dos dois tipos de estressores conseguiu levar os animais à anedonia (queda na preferência por sacarose). No entanto, ao observar o ganho de peso dos animais ao longo do tempo e o mapeamento cerebral com citocromo c oxidase, notamos que o estresse teve seu impacto no animais. Comparados a outros modelos de depressão, o CMS tem a premissa de desenvolver um estado depressivo nos animais antes do teste com drogas antidepressivas, fazendo com que tenha uma alta validade preditiva. Ele também pode incorporar outros endpoints para avaliar outros comportamentos, além da anedonia, que possam demonstrar o estado depressivo no animal. Por exemplo, observamos no mapeamento cerebral que a substância negra e a PAG estiveram mais ativas no estresse físico e elas podem estar implicadas na busca por recompensa e na modulação de dor, respectivamente. Concluímos que o modelo de CMS é apropriado, embora ainda necessite de estudos quanto à equivalência de intensidade de estressores
Major Depressive Disorder (MDD) is a widespread disease all over the world with a high prevalence, especially among women. Mood disorders are recurrent and life threatening, due to suicide risk. Despite those, MDD etiology is poorly understood and several hypotheses have been developed to try and explain it. One of them is connected to stress. Disorders on the hypothalamus-pituitary-adrenal (HPA) axis are present in up to 70% of patients with depression. While searching for a better animal model to study the impact that stress might have on depression onset, we came across the Chronic Mild Stress (CMS) model. During previous studies developed in this lab, weve observed that there are differences between types of stressors and mediators involved in the HPA axis response, i.e. during physical stress, the mediator secreted is vasopressin, whereas during psychological stress, the mediator is CRF; on mixed stress (like forced swim), both mediators are present. That way, we proposed to set up CMS protocols based on Paul Willner (the researcher who developed this model)s original one, employing physical or psychological stressors separately. None of the types of stressors were able to induce anhedonia (decrease in sucrose preference) in the animals. However, noticing the animals weight gain over time, and cerebral mapping with cytochrome c oxidase, we could see that stress had impact over the animals. Compared to other depression models, CMS has the presupposition of leading the animals to a depressive-like state before testing antidepressant drugs, which gives it a high predictive validity. The model can also incorporate different endpoints to assess other behaviors, besides anhedonia, that may show the animals depressive-like state. For instance, we observed in the brain mapping that substantia nigra and PAG were more activated in physical stress and they can be implicated in reward seeking and pain modulation, respectively. So, we conclude that the CMS model is appropriate, although it still needs more research regarding the intensity of stressors equivalence

Thesis (PhD)--Stellenbosch University, 2014.
ENGLISH ABSTRACT: Posttraumatic stress disorder (PTSD) is a severe, chronic and debilitating psychiatric disorder that can present after the experience of a life-threatening traumatic event. D-cycloserine (DCS), a partial N-methyl-D-aspartate (NMDA) receptor agonist, has been found to augment cognitive behavioural therapy by facilitating fear extinction; however, the precise mechanisms whereby DCS ameliorates fear triggered by a traumatic context remains to be fully elucidated. This study aimed to (i) identify the molecular mechanisms of intrahippocampally administered DCS in facilitating fear extinction in a rat model of PTSD by investigating gene expression profiles in the left dorsal hippocampus (LDH) of male Sprague Dawley rats and (ii) determine whether microRNA (miRNA) expression and DNA methylation mediated these gene expression changes. An adapted version of the PTSD animal model described by Siegmund and Wotjak (2007) was utilised. The total number of 120 rats were grouped into four experimental groups (of 30 rats per group) based on fear conditioning and the intrahippocampal administration of either DCS or saline: (1) fear conditioned + intrahippocampal saline administration (FS), (2) fear conditioned + intrahippocampal DCS administration (FD), (3) control + intrahippocampal saline administration (CS) and (4) control + intrahippocampal DCS administration (CD). Behavioural tests (the light/dark [L/D] avoidance test, forced swim test and open field test) were conducted to assess anxiety and PTSD-like behaviours. The L/D avoidance test was the most sensitive behavioural test of anxiety and was subsequently used to differentiate maladapted (animals that displayed anxiety-like behaviour) and well-adapted (animals that did not display anxiety-like behaviour) subgroups. In order to identify genes that were differentially expressed between FS maladapted (FSM) (n = 6) vs. FD well-adapted (FDW) (n = 6) groups, RNA sequencing was performed on the Illumina HiSeq 2000 which generated more than 60 million reads per sample. This was followed by subsequent bioinformatics analyses (using the software programs TopHat, Bowtie, Cuffdiff and Bio-Ontological Relationship Graph (BORG) database (that identifies genes that may be biologically relevant) to identify biologically relevant differentially expressed genes between the treatment groups. Epigenetic mechanisms mediating observed differences in gene expression were investigated by conducting DNA methylation and miRNAseq analyses in the FDW and FSM experimental groups. DNA methylation was investigated using real-time quantitative PCR (qPCR) amplification followed by high resolution melt analysis on the Rotor-GeneTM 6000. Differences in miRNA expression levels between the FDW and FSM groups were investigated by sequencing the miRNA fraction on the MiSeq platform. The bioinformatics pipeline used to analyse the RNAseq data identified 93 genes that were significantly downregulated in the FDW group compared to the FSM group. Forty-two of these genes were predicted to be biologically relevant (based on BORG analysis). Integrative network analyses revealed subsets of differentially expressed genes common across biological functions, pathways and disorders. The co-administration of DCS and behavioural fear extinction downregulated immune system genes and genes that transcribe proinflammatory and oxidative stress molecules. These molecules mediate neuroinflammation and subsequently cause neuronal damage. DCS also regulated genes involved in learning and memory processes. Additionally, a subset of the genes, which have been found to be associated with disorders that commonly co-occur with PTSD (such as cardiovascular disease, metabolic disease, Alzheimer‘s and Parkinson‘s disease), was downregulated by the co-administration of DCS and behavioural fear extinction. In order to determine whether real-time qPCR analysis would be sensitive enough to detect differential expression in those genes found to be differentially expressed in RNAseq analysis, the expression of nine genes was analysed using SYBR Green qPCR technology. In the LDH, six of the nine genes were found to be differentially expressed between FDW and FSM groups and one gene, matrix metallopeptidase 9 (MMP9), was observed to be differentially expressed between these two groups in the blood. Three of the nine genes for which differential expression levels were investigated using SYBR Green real-time qPCR, contained CpG islands and were used for CpG island DNA methylation analysis. Results indicated that CpG island DNA methylation did not mediate differential gene expression of TRH, NPY or MT2A. Bioinformatics analysis of miRNAseq data identified 23 miRNAs that were differentially expressed between the FDW and FSM groups. Several of these miRNAs have previously been found to be involved in brain development and behavioural measures of anxiety. Furthermore, functional luciferase analysis indicated that the upregulation of rno-mi31a-5p could have facilitated the downregulation of interleukin 1 receptor antagonist gene (IL1RN) as detected in RNAseq. RNAseq and miRNAseq analyses in this PTSD animal model identified differentially expressed genes and miRNAs that serve to broaden our understanding of the mechanism whereby DCS facilitates fear extinction. To this end, immune system genes and genes transcribing proinflammatory and oxidative stress molecules were among the genes that were found to be differentially expressed between the FDW and FSM groups. Based on the results obtained, it can be hypothesised that DCS attenuates neuroinflammation and subsequent neuronal damage, and also regulates genes involved in learning and memory processes. Concomitantly, these gene expression alterations mediate optimal neuronal functioning, plasticity, learning and memory (such as fear extinction memory) which contribute to the fear extinction process. Furthermore, biologically relevant differentially expressed genes that were associated with DCS facilitation of fear extinction and with other chronic medical conditions, such as cardiovascular disease and metabolic diseases, might help to explain the co-occurrence of these disorders with PTSD. In conclusion, Identifying the molecular underpinnings of DCS-mediated fear extinction brings us closer to understanding the process of fear extinction and could, in future work be used to explore novel therapeutic targets to effectively treat PTSD and related disorders.
AFRIKAANSE OPSOMMING: Posttraumatiese stressindroom is 'n ernstige, kroniese aftakelende psigiatriese toestand wat kan ontwikkel na 'n lewensgevaarlike traumatiese gebeurtenis. Daar is bevind dat die gesamentlike toediening van D-sikloserien (DCS), 'n N-metiel-D-aspartaat (NMDA) reseptor agonis, en kognitiewe gedragsterapie effektief is in die bemiddeling van vrees uitwissing; maar die presiese meganisme waar deur DCS die vrees wat deur 'n traumatiese konteks ontlok word verminder, is egter onduidelik. Hierdie studie het beoog om (i) die molekulêre meganismes te identifiseer waardeur intra-hippokampaal toegediende DCS vrees uitwissing fasiliteer, in 'n rot model van posttraumatiese stressindroom, deur geen uitdrukkingsprofiele in the linker dorsale hippokampus (LDH) van manlike Sprague Dawley rotte te ondersoek en (ii) om te bepaal of mikroRNA (miRNA) uitdrukking en DNA metilering die veranderinge in geen uitdrukking bemiddel het. 'n Gewysigde weergawe van die posttraumatiese stressindroom diere model, beskryf deur Siegmund en Wotjak (2007), was gebruik tydens die studie. Rotte was in vier groepe verdeel, vrees kondisionering + soutwater (FS), vrees kondisionering + DCS (FD), kontrole + soutwater (CS) en kontrole + DCS (CD). Gedragstoetse was uitgevoer om angstige, vreesvolle en posttraumatiese stressindroom-tipe gedrag te evalueer. Gedurende die lig/donker (L/D) vermydingstoets het die FS groep aansienlik meer tyd in die donker kompartement deurgebring ('n indikasie van vreesvolle gedrag) in vergelyking met die CS en die FD groepe wat meer tyd in die verligte kompartement deurgebring het ('n indikasie van vreeslose gedrag). Die L/D toets was die mees sensitiewe gedragstoets vir angstige en vreesvolle gedrag en was gevolglik gebruik om die diere te sub-groepeer in wanaangepaste (diere wat angstige en vreesvolle gedrag vertoon het) en goedaangepaste (diere wat nie angstige en vreesvolle gedrag vertoon het nie) subgroepe. Nuwe generasie RNA volgordebepaling (RNAseq) van die LDH RNA en daaropvolgende bioinformatiese analise was uitgevoer om gene te identifiseer wat differensieel uitgedruk is tussen die twee behandelingsgroepe van belang in die betrokke studie, naamlik FS wanaangepaste (FSM) teenoor FD goedaangepaste (FDW) groepe. Epigenetiese analises was uitgevoer om te bepaal of differensieel uitgedrukte miRNAs of CpG-eiland DNA metilasie die differensiële geenuitdrukking bemiddel het. Bioinformatiese analises van die RNAseq data het 93 gene geïdentifiseer waarvan die geen uitdrukking beduidend onderdruk was in die FDW groep in vergelyking met die FSM groep; 42 van hierdie gene was voorspel om biologies relevant te wees. Geïntegreerde netwerk analise het onthul dat sekere van die differensieel uitgedrukte gene gemeenskaplik was tussen verskeie biologiese funksies, padweë en versteurings. DCS het die uitdrukking van immuun-sisteem gene en pro-inflammatoriese en oksidatiewe stres gene verlaag. Hierdie molekules medieer neuro-inflammasie wat gevolglik tot neurale skade lei. DCS het ook gene gereguleer wat betrokke is by leer en geheue prosesse. DCS het onder meer ook die geenuitdrukking verlaag van 'n sub-groep van gene wat voorheen geassosier is met komorbiede versteurings van PTSD. SYBR Green real-time qPCR (werklike tyd kwantitatiewe polimerase ketting reaksie) analise was ondersoek om te bepaal of hierdie metode sensitief genoeg sou wees om die verlaagde geen-uitdrukking van verskeie van die biologies relevante differensieel uitgedrukte gene te identifiseer, in dieselfde LDH komplementêre DNA (cDNA) monsters as wat in die RNAseq gebruik is, asook in die bloed cDNA monsters. SYBR Green real-time qPCR was in staat om ses, van die nege, differensieel uitgedrukte gene in die LDH cDNA monsters en een geen, matriks metallopeptidase 9 (MMP9), in die bloed cDNA monsters op te tel. Drie van die gene waarvoor SYBR Green real-time qPCR gebruik is om differensiële geenuitdrukking te toets, het CpG eilande bevat en was gevolglik gebruik in CpG eiland DNA metilering analises. Resultate het getoon dat CpG eiland DNA metilering nie die differensiële geenuitdrukking van TRH, NPY of MT2A gedryf het nie. Bioinformatiese analises van die miRNAseq data het 23 miRNAs geïdentifiseer wat differensieël uitgedruk was tussen die FDW en FSM groepe. Verskeie van hierdie miRNAs is reeds voorheen beskryf om betrokke te wees in brein ontwikkeling en angs gedrags metings. Funksionele luciferase analises het verder aangedui dat die verhoogde uitdrukking van rno-mi31a-5p moontlik die verlaagde geen uitdrukking van IL1RN, soos waargeneem in die RNAseq data, kon bewerkstellig het. RNAseq en miRNAseq analises in hierdie posttraumatiese stressindroom dieremodel het differensieël uitgedrukte gene en miRNAs geïdentifiseer wat dien om die verstaanswyse te verbreed van hoe DCS die vrees uitwissings proses fasiliteer. Die meganismes waardeur DCS vrees uitwissings bewerkstellig het sluit die verlaging van immuun-sisteem geen-uitdrukking in, sowel as verlaagde uitdrukking van gene wat pro-inflammatoriese en oksidatiewe stress gene transkribeer. DCS het daardeur neuro-inflammasie en gevolglike neurale skade voorkom. DCS het daarmee saam ook gene gereguleer wat betrokke is by leer en geheue prosesse. Hierdie gesamentlike veranderings in geen uitdrukking het gelei tot die uiteindelike bewerkstelling van optimale neurale funksionering, plastisiteit, leer en geheue prosesse wat uiteindelik bygedra het tot vrees uitwissing. Biologies relevante differensieël uitgedrukte gene wat ook geassosieer was met ander kondisies, soos middel verwante versteurings en metaboliese versteurings, kan help om die komorbiditeit met posttraumatiese stressindroom te verklaar. Identifisering van die molekulêre grondslae van DCS bemiddelde vrees uitwissing verbreed ons begrip en verstaan van vrees uitwissing en kan moontlik, in toekomstige navorsing gebruik word om nuwe innoverende terapeutiese teikens te verken om sodoende posttraumatiese stressindroom meer effektief te kan behandel.

This thesis, divided into two parts, is concerned with the analysis of spectral and dynamical characteristics of certain quantum spin systems in the presence of either I) quenched disorder, or II) dynamical noise. In the first part, the quantum random energy model (QREM), a mean-field spin glass model with a many-body localisation transition, is studied. In Chapter 2, we attempt a diagrammatic perturbative analysis of the QREM from the ergodic side, proceeding by analogy to the single-particle theory of weak localisation. Whilst we are able to describe diffusion, the analogy breaks down and a description of the onset of localisation in terms of quantum corrections quickly becomes intractable. Some progress is possible by deriving a quantum kinetic equation, namely the relaxation of the one-spin reduced density matrix is determined, but this affords little insight and extension to two-spin quantities is difficult. We change our approach in Chapter 3, studying instead a stroboscopic version of the model using the formalism of quantum graphs. Here, an analytic evaluation of the form factor in the diagonal approximation is possible, which we find to be consistent with the universal random matrix theory (RMT) result in the ergodic regime. In Chapter 4, we replace the QREM's transverse field with a random kinetic term and present a diagrammatic calculation of the average density of states, exact in the large-N limit, and interpret the result in terms of the addition of freely independent random variables. In the second part, we turn our attention to noisy quantum spins. Chapter 5 is concerned with noninteracting spins coupled to a common stochastic field; correlations arising from the common noise relax only due to the spins' differing precession frequencies. Our key result is a mapping of the equation of motion of n-spin correlators onto the (integrable) non-Hermitian Richardson-Gaudin model, enabling exact calculation of the relaxation rate of correlations. The second problem, addressed in Chapter 6, is that of the dynamics of operator moments in a noisy Heisenberg model; qualitatively different behaviour is found depending on whether or not the noise conserves a component of spin. In the case of nonconserving noise, we report that the evolution of the second moment maps onto the Fredrickson-Andersen model - a kinetically constrained model originally introduced to describe the glass transition. This facilitates a rigorous study of operator spreading in a continuous-time model, providing a complementary viewpoint to recent investigations of random unitary circuits.

Thesis (Ph. D.)--University of Oregon, 1999.
Typescript. Includes vita and abstract. Includes bibliographical references (leaves 165-166). Also available for download via the World Wide Web; free to University of Oregon users. Address: http://wwwlib.umi.com/cr/uoregon/fullcit?p9948028.

The aims of the current research program were to examine the social-cognitive and sociological models of stigma in relation to student attitudes towards an individual experiencing a mood disorder. Two experiments (Studies 1 and 2) sought to empirically distinguish between controllability and responsibility, both constructs of the attribution model which is subsidiary to the social-cognitive model of stigma. Despite manipulating controllability, participants were reluctant to attribute controllability of cause to individuals experiencing depression or bipolar disorder. The stability of beliefs about the controllability of cause for condition onset was consistent with research suggesting that the Australian public increasingly conceptualise mental disorders in terms of biochemical and genetic causal factors. These findings, in combination with past research linking biogenetic beliefs to negative attitudes, resulted in a change in focus of investigation in Studies 3, 4, 5 and 6 to explain why, contrary to the prediction of the attribution model, biogenetic explanations of mental disorders are associated with the proliferation of stigma. To measure causal beliefs, the Causal Belief Inventory (CBI) was developed in Study 3 and refined in Study 4. The correlational results examined in Studies 4, 5 and 6 found that genetic and biochemical causal beliefs were associated with a number of positive attitudes towards individuals experiencing a mood disorder and that genetic cause was associated with a reduced implicit bias against major depression. Furthermore, each study pointed to the centrality of judgments of differentness in determining affective responses and direct and proxy measures of behaviour. In contrast, manipulation of genetic and psychosocial cause in Study 5 found that causal condition largely failed to impact upon student attitudes. Mediator analysis did, however, find that beliefs about the stability of the vignette actor's condition fully mediated the relationship between the negative influence of genetic cause on proxy helping behaviour. Manipulation of psychosocial, genetic and biochemical cause with the inclusion of a non-depressed control in Study 6 resulted in more ambiguous findings. The combination of findings from Studies 1 to 6 suggest that focusing on the impact of the controllability of cause of depression onset on student attitudes is unwarranted. Instead researchers and public health educators should be examining models which facilitate the examination of the cognitive factors that mediate these relationships. Two such models, namely the social-cognitive and sociological models of stigma, were found to adequately fit the data. Recommendations for integrating these two models of stigma are discussed.

This thesis contains four studies of the effects of disorder and randomness on strongly correlated quantum phases of matter. Starting with an itinerant ferromagnet, I first use an order-by-disorder approach to show that adding quenched charged disorder to the model generates new quantum fluctuations in the vicinity of the quantum critical point which lead to the formation of a novel magnetic phase known as a helical glass. Switching to bosons, I then employ a momentum-shell renormalisation group analysis of disordered lattice gases of bosons where I show that disorder breaks ergodicity in a non-trivial way, leading to unexpected glassy freezing effects. This work was carried out in the context of ultracold atomic gases, however the same physics can be realised in dimerised quantum antiferromagnets. By mapping the antiferromagnetic model onto a hard-core lattice gas of bosons, I go on to show the importance of the non-ergodic effects to the thermodynamics of the model and find evidence for an unusual glassy phase known as a Mott glass not previously thought to exist in this model. Finally, I use a mean-field numerical approach to simulate current generation quantum gas microscopes and demonstrate the feasibility of a novel measurement scheme designed to measure the Edwards-Anderson order parameter, a quantity which describes the degree of ergodicity breaking and which has never before been experimentally measured in any strongly correlated quantum system. Together, these works show that the addition of disorder into strongly interacting quantum systems can lead to qualitatively new behaviour, triggering the formation of new phases and new physics, rather than simply leading to small quantitative changes to the physics of the clean system. They provide new insights into the underlying physics of the models and make direct connection with experimental systems which can be used to test the results presented here.

The Five Factor Obsessive Compulsive Inventory (FFOCI) was developed in part to facilitate a shift from the categorical classification of personality disorder to a dimensional model; more specifically, the five-factor model. Questions though have been raised as to whether obsessive-compulsive personality disorder can be understood as a maladaptive variant of FFM conscientiousness. The purpose of the present study was to provide a further validation of the FFOCI, as well as to compare and contrast alternative measures and models of OCPD. A total of 380 participants, including 146 oversampled for OCPD traits, were recruited from introductory psychology courses at the University of Kentucky. Administered were the FFOCI, measures of general personality (e.g.,, International Item Pool, 5-Dimensional Personality Test), trait scales associated with OCPD (e.g.,, workaholism, compulsivity, propriety), and alternative measures of obsessive compulsive personality disorder. All measures were administered via SurveyMonkey, a secure online survey service. Results supported the validity of the FFOCI, but also demonstrated substantive differences among the alternative measures of OCPD, particularly with respect to their relationship with FFM conscientiousness, antagonism, and introversion.

Psychology
Ph.D.
Most life stress literature in bipolar disorder (BD) fails to account for the possibility of a changing relationship between psychosocial context and episode initiation across the course of the disorder. The kindling hypothesis states that over the longitudinal course of recurrent affective disorders, there is a weakening temporal relationship between major life stress and episode initiation (Post, 1992). This process could reflect either a progressive sensitization or a progressive autonomy (i.e., insensitivity) to life stress. The present study aimed to test the kindling model in BD by examining the effect of lifetime mood episodes on the relationship between proximal life events and prospectively assessed mood episodes. Polarity-specific tests of the model were conducted across the continuum of event severity, with respect to both impact and frequency of life events. Moreover, examination of the kindling hypothesis was embedded in the context of two emerging biopsychosocial theories of BD: the expanded Behavioral Approach System Dysregulation Model and the Circadian and Social Rhythm Theory. Data from 278 participants (146 bipolar spectrum participants and 132 normal control participants) were collected as part of the Temple-Wisconsin Longitudinal Investigation of Bipolar Spectrum Project. Hypotheses were polarity- and event-type specific and were in line with a stress sensitization model of bipolar spectrum disorders (BSD), rather than a stress autonomy model. Results partially supported a sensitization model: there was a decreased frequency and an increased impact of major events, and an increased frequency and impact of minor events. However, results for specific polarities and event types were not fully consistent with a stress sensitization model. Implications of these findings are addressed, followed by a discussion of study strengths, limitations, and promising directions for future research.
Temple University--Theses

Condensed matter systems undergoing phase transitions rarely allow exact solutions. The presence of disorder renders the situation  even worse but collective Monte Carlo methods and parallel algorithms allow numerical descriptions. This thesis considers classical phase transitions in disordered spin systems in general and in effective models of superfluids with disorder and novel interactions in particular. Quantum phase transitions are considered via a quantum to classical mapping. Central questions are if the presence of defects changes universal properties and what qualitative implications follow for experiments. Common to the cases considered is that the disorder maps out correlated structures. All results are obtained using large-scale Monte Carlo simulations of effective models capturing the relevant degrees of freedom at the transition. Considering a model system for superflow aided by a defect network, we find that the onset properties are significantly altered compared to the $\lambda$-transition in $^{4}$He. This has qualitative implications on expected experimental signatures in a defect supersolid scenario. For the Bose glass to superfluid quantum phase transition in 2D we determine the quantum correlation time by an anisotropic finite size scaling approach. Without a priori assumptions on critical parameters, we find the critical exponent $z=1.8 \pm 0.05$ contradicting the long standing result $z=d$. Using a 3D effective model for multi-band type-1.5 superconductors we find that these systems possibly feature a strong first order vortex-driven phase transition. Despite its short-range nature details of the interaction are shown to play an important role. Phase transitions in disordered spin models exposed to correlated defect structures obtained via rapid quenches of critical loop and spin models are investigated. On long length scales the correlations are shown to decay algebraically. The decay exponents are expressed through known critical exponents of the disorder generating models. For cases where the disorder correlations imply the existence of a new long-range-disorder fixed point we determine the critical exponents of the disordered systems via finite size scaling methods of Monte Carlo data and find good agreement with theoretical expectations.

QC 20150306