Thesis (Ph.D.)--Fairleigh Dickinson University, 2000. / Source: Dissertation Abstracts International, Volume: 61-02, Section: B, page: 1066. Chairperson: Christopher A. Capuano. Available also in print.

Thesis (Psy.D.)--Fairleigh Dickinson University, 2004. / Source: Dissertation Abstracts International, Volume: 65-01, Section: B, page: 0458. Chair: Ron Dumont. Available also in print.

Thesis (Ph.D.)--Fairleigh Dickinson University, 2004. / Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 2117. Chairperson: Lana Tiersky. Available also in print.

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This thesis examines how Shia Muslims react to sudden, unexplained, and prolonged pain. In doing so, the thesis frames physical pain not only as physiological phenomenon but also as a phenomenon that is defined by historical, cultural and social context. Sudden, unexplained and prolonged pain not only produces physical hurt, it also has the capacity to interrupt individuals' social activities and as a consequence their identities and the meanings with which they are associated. For this reason, it is argued that biomedicine and psychology are not always capable of giving satisfactory accounts of the experience of pain. This failure frequently leads individuals who succumb to sudden, unexplained and prolonged pain to look for meaning in religious or quasi-religious experience. The thesis first explores historically divergent conceptions of pain. It then gives an overview of biomedical, psychological and sociological and anthropological conceptions of pain. A theoretical framework is developed that connects the experience of pain with broader social meanings, identity and the body. This framework is used to analyse qualitative data collected through semi-structured interviews with Shia Muslim scholars and Shia Muslim respondents who have experienced or are experiencing sudden unexplored pain. It is shown that the religious worldview provides believers with cultural resources that allow them to negotiate the crisis of meaning and identity provoked by the experience of sudden, unexplained, prolonged pain.

Corticotropin-releasing hormone (CRH) has been considered the quintessential 'stress' neuropeptide, as it mediates stress-induced activation of the hypothalamic-pituitary-adrenal (HPA) axis and produces behavioural and autonomic responses analogous to natural stressors. However, the role of CRH in mediating the behavioural response to psychological stressors, also termed anxiety, is unclear due to inconsistent anxiolytic effects for CRH antagonists in processive stress models, and the central activation of CRH by non-anxiogenic stimuli. The first half of the current thesis examined the role of CRH, and amygdala CRH in particular, in the behavioural response to anxiety. The first experiment standardized the use of a neophobia-based feeding model for use as a behavioural index of anxiety. Using this model, the second experiment demonstrated that while exposure to an unfamiliar environment activates stress-relevant neural circuitry, activation of CRH receptors is not necessary for the expression of anxiety-like behavioral responses. In addition, amygdala CRH activation by novel stimuli is unaffected by changes in the organism's anxiety state. The second half of the current thesis focused on the role of CRH in neurotoxicity and behavioural deficits produced by global ischemic insults. It was demonstrated that global ischemic insults of 10--15 min duration produced short-term CRH increases in hypothalamic and amygdalar regions as well as the piriform cortex, perhaps mediating stress, inflammatory and/or epileptiform activity. This was followed by widespread CRH depletions throughout the brain at 24 h post-ischemia. However, by 72 h post-ischemia, just prior to the onset of cell death, CRH concentrations had normalized throughout the brain. Furthermore, there were no short or long term CRH changes at the CA1 hippocampal region, the area most vulnerable to cell death. Both selective and non-selective CRH antagonists failed to confer neuroprotection when administered before or shortly after an ischemic insult, and failed to protect against ischemia-induced spatial memory deficits. However, CRH1 antagonists did significantly attenuate ischemia-induced hyperactivity in the open field and in the elevated plus maze. Thus while ischemia-induced CRH activation does not appear to mediate subsequent neuronal degeneration, it may play a role in anxiety-related behavioural changes.

L'objectif principal de cette these etait de caracteriser l'impact d'une consommation alimentaire quotidienne reduite en calorie ou enrichie de gras polyinsatures (PUFA) sur les repercussions neuronales et fonctionnelles d'une ischemie cerebrale globale. Differents groupes de rats furent assignes aleatoirement aux conditions experimentales, determinees par la diete consommee et la procedure chirurgicale administree. Les regimes alimentaires des deux premieres etudes de cette these incluaient l'ingestion alimentaire ad libitum ou une restriction alimentaire de 40% comparee a l'ingestion des rats des groupes ad libitum. Dans une troisieme etude, nous avons evalue l'impact de la consommation d'une diete enrichie de gras polyinsatures de type omega 3 et omega 6, via l'ajout de 11.5% d'huile de poisson et de 3.5% d'huile de mais a la diete controle. Ces differentes dietes furent toutes initiees chez des rats ages de 4 semaines et maintenues pendant une periode de 18 semaines (pre et post-chirurgie). Les procedures chirurgicales, administrees durant la 13ieme semaine d'ingestion alimentaire, incluaient soit une chirurgie vasculaire impliquant 8 ou 12 minutes d'ischemie cerebrale globale ou une operation controle (chirurgie sham). Suite a ces procedures, l'administration d'une serie de paradigmes comportementaux debuta pour l'ensemble des animaux au 4ieme ou 5ieme jour suivant la chirurgie, et se terminant 7, 31 ou 70 jours suivant l'ischemie, dependamment de l'experimentation. Les tests comportementaux utilises incluaient l'aire ouverte, le labyrinthe en croix et le labyrinthe radial a huit bras. A l'instar des recherches suggerant des effets neuroprotecteurs de la restriction alimentaire et de l'ingestion de supplements d'acides gras polyinsatures, nos resultats demontrent que la survie neuronale dans le CA1 de l'hippocampe est comparable entre les rats ischemies nourris des dietes experimentales et ceux nourris a volonte. Cette absence de difference s'observe 7, 31 et 70 jours suivant la procedure chirurgicale. Egalement, nos resultats comportementaux revelent une reduction significative, voire la prevention, des deficits d'apprentissage et de memoire spatiale induits par l'ischemie globale chez les rats restreints et nourris d'une diete enrichie de PUFA. Les performances mnesiques de ces animaux sont comparables a celle des rats controles et significativement meilleure que celle des rats ischemies nourris d'une diete reguliere. Fait plus impressionnant, les animaux ischemies restreints demontrent egalement la capacite de completer une serie de taches differees complexes appariees ou non a l'echantillon (DMTS/DNMTS) dans le labyrinthe radial, contrairement aux rats ischemies nourris a volonte. Nos resultats suggerent que la restriction alimentaire et l'ingestion de supplements d'acides gras polyinsatures induisent des changements plastiques et/ou l'activation de mecanismes endogenes compensatoires capables de proteger les animaux des deficits d'apprentissage et de memoire spatiale generalement produits par l'ischemie globale.