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1

Dolan, Mary L. "Living with Alzheimer's Disease: An Examination of Caregiver Coping Mechanisms." Ohio University Honors Tutorial College / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ouhonors1276009587.

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2

Sirois, Fuschia M., and Jameson K. Hirsch. "A Longitudinal Study of the Profiles of Psychological Thriving, Resilience, and Loss in People With Inflammatory Bowel Disease." Digital Commons @ East Tennessee State University, 2017. https://doi.org/10.1111/bjhp.12262.

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Objectives: Despite the toll of inflammatory bowel disease (IBD) on adjustment, many patients are resilient to the challenges associated with living with IBD, and successfully cope with their illness and thrive. Yet there is little research on why some individuals with IBD enter a trajectory of growth, while others may struggle to adapt. The aim of this study was to investigate the adjustment‐related factors that distinguished thriving, resilience, and loss in people with IBD across personal growth, life satisfaction, and relationship quality domains. Design: Prospective cohort design with two data collection points, 6 months apart. Methods: From a sample of 420 people with active IBD who completed an online survey, 152 participants completed the follow‐up survey and were included in the analyses. Participants completed measures of thriving, and cognitive, affective, social, and disease‐related variables known to predict adjustment. Results: Time 1 ANCOVAs and pairwise comparisons controlling for demographics distinguished loss from resilience and thriving on the four outcomes – coping efficacy, illness acceptance, depressive symptoms, and perceived social support – for all three domains. Time 2 ANCOVAs and pairwise comparisons controlling for baseline outcomes revealed that the Time thriving categories predicted differences in Time 2 adjustment, mainly for the life satisfaction domain, with those experiencing loss reporting poorer adjustment than those experiencing resilience and thriving. Conclusions: Findings highlight the distinctions among profiles of thriving, resilience, and loss in adjustment to IBD, and suggest that strategies that enhance coping and address depressive symptoms may optimize thriving in the context of IBD.
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3

Leung, Yiu-por, and 梁耀波. "Coping strategies of cardiovascular disease patients." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1996. http://hub.hku.hk/bib/B31978125.

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4

Hardy, Rachel Margaret. "Coping and awareness in Alzheimer's disease." Thesis, University of Birmingham, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.420420.

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5

Leung, Yiu-por. "Coping strategies of cardiovascular disease patients." Hong Kong : University of Hong Kong, 1996. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19470125.

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6

Ramsey, Nina Sharp. "Caregiver coping with dementia : relationships among patient characteristics, caregiver coping styles, and consequences of caregiving /." Thesis, Connect to this title online; UW restricted, 1990. http://hdl.handle.net/1773/11178.

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7

Schlindwein, Helena E. M. "Alternative stress coping mechanisms in conflict situations." Thesis, University of Ulster, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242241.

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8

Miller, Aaron. "Black Band Disease: Elucidating Origins and Disease Mechanisms." FIU Digital Commons, 2012. http://digitalcommons.fiu.edu/etd/558.

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Coral diseases were unknown in the scientific community fifty years ago. Since the discovery of a coral disease in 1965, there has been an exponential increase in the number of known coral diseases, as the abundance, prevalence, distribution, and number of host species affected has also significantly increased. Coral diseases are recognized as contributing significantly to the dramatic losses of coral cover on a global basis, particularly in the Caribbean. The apparent sudden emergence of coral diseases suggests that they may be a symptom of an overall trend associated with changing environmental conditions. However, not much evidence has been gathered to address this question. The following studies were designed to build a comprehensive argument to support this hypothesis for one important coral disease – black band disease (BBD). A meta-analysis of clone libraries identifying the microbial communities associated with BBD reveal important information including that a single cyanobacterial operational taxonomic unit (OTU) was by far the most prevalent OTU in diseased samples, and that the alphaproteobacteria, which include some of the most common bacteria in marine waters, were the most diversely represented. The analysis also showed that samples exhibited regional similarities. An fine and ultrastructural characterization of the disease revealed that the cyanobacteria are prolific borers through the coral skeleton, and that the cyanobacteria penetrate coral tissue, leading to their presence ahead of the main migrating disease band. It was further found that apparently healthy corals exposed to toxins found in BBD, exhibited similar tissue degradation to those infected with BBD. Comparing the disease progression to biofilm formation, it was determined that scouting cyanobacteria may contribute to the migration of the disease through progressive biofilm development over intact coral tissue. Together, these studies provide significant evidence for the hypothesis that BBD is an opportunistic disease, caused by common environmental bacteria, facilitated by the changing environmental conditions associated with climate change.
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9

Schulz, Katharine I. "Coping strategies in coronary artery disease patients." Virtual Press, 1993. http://liblink.bsu.edu/uhtbin/catkey/862273.

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10

O'Regan, David. "Mechanisms of glucocorticoid programmed disease." Thesis, University of Edinburgh, 2004. http://hdl.handle.net/1842/27148.

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This thesis investigates the role of the renin-angiotensin (RAS), and sympathetic nervous systems (SNS) in determining programmed hypertension, and further seeks to determine whether programming effects are sexually dimorphic. DEX administration in the last week of gestation reduces offspring birth weight and programmes adult cardiovascular and metabolic physiology in a sex specific manner. In male offspring, prenatal glucocorticoid exposure programmes elevated basal circulating corticosterone, elevated PEPCK activity, and produces adulthood postglucose hyperglycaemia and hyperinsulinaemia. Whilst in female offspring, prenatal DEX programmes elevated hepatic angiotensinogen mRNA expression, elevated plasma angiotensinogen and renin activity, and produces hypertension, when measured by tail-cuff plethysmography. Unlike previous studies, offspring blood pressure was subsequently assessed with radiotelemetry, which is unmarred by any stress artefact. We no demonstrate that prenatal DEX-treated male and female offspring actually display <i>lower</i> basal blood pressure in adulthood; with the commonly expected hypertensive phenotype only being noted when these offspring are subjected to any stressor. Moreover, DEX-treated offspring sustain their stress-induced hypertension for longer. These hypertensive responses are mediated by alterations in the responsitivity of the sympathetic nervous system, being ameliorated by the inhibition of catecholamine synthesis, and further exaggerated by the promotion of systemic catecholamine release. Additionally, we demonstrate that DEX-treated offspring display greater sensitivity to various vasoconstrictors in the isolated mesenteric vasculature. These findings demonstrate that <i>in utero </i>over-exposure to glucocorticoids actually results in stress-induced hypertension, and support a role for both RAS and SNS in mediating this. Furthermore, it appears that the programming of cardiovascular physiology may reflect distinct processes in each gender, whilst the programming of metabolic physiology is male specific.
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11

Palmer, Samantha Jane. "Compensatory mechanisms in Parkinson's disease." Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/22661.

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Parkinson’s disease (PD) is a common movement disorder, affecting 1% of the population over the age of 65. Pathologically, PD results from degeneration of nigral dopaminergic neurons, however symptoms do not appear until an estimated 50% of these cells are lost, suggesting compensatory mechanisms exist which mask disease onset, and may later delay progression of the disease. Compensation may take place over various spatial and temporal scales, from changes in synaptic dopamine release and synthesis that take place over a period of minutes, to recruitment of novel, widespread networks of brain regions for a specific task, which may require formation of new connections over an extended period of time. Neuroimaging techniques have recently allowed the investigation of regional and network changes in activation related to motor performance in PD, however the question of whether such changes represent a downstream effect of basal ganglia degeneration, or a compensatory change, remains difficult to determine. Here, we applied an approach from research into Alzheimer’s Disease, where abnormal activation patterns are studied in the context of tasks of increasing difficulty, such that inferences regarding their compensatory nature can be made. We show that individuals with PD are able to increase the recruitment of normal networks for a motor task (motor reserve) as a form of compensation, in addition to compensatory recruitment of novel networks to accomplish the same task as healthy controls. In particular, we observe a switch from striato-thalamo-cortical (STC) motor loops to cerebello-thalamo-cortical (CTC) loops as a compensatory strategy. This compensatory recruitment involves changes in the amplitude, spatial extent, and connectivity of regions within the CTC pathway. However, this compensation does not come without a price, since we show that compensatory CTC recruitment involving disconnection between the STC and CTC loops occurs in subjects with tremor-dominant PD, but not akinetic-rigidity-dominant PD, supporting a growing body of evidence that suggests the cerebellum plays an important role in the generation of PD tremor. Together, this body of research has implications for treatments that target the symptom of tremor in PD, as therapies which minimize tremor might also reduce beneficial aspects of compensation.
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12

Zhang, Li. "Immunological mechanisms in autoimmune disease." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308276.

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13

Bourne, Nathan T. "Molecular mechanisms of Alzheimer's disease." Thesis, University of Sheffield, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.521906.

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14

Freeburn, Jennifer. "Haemostatic mechanisms in vascular disease." Thesis, University of Ulster, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390118.

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15

Freese, Andrew. "Excitotoxic mechanisms in Huntington's disease." Thesis, Massachusetts Institute of Technology, 1991. http://hdl.handle.net/1721.1/17295.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Whitaker College of Health Sciences and Technology, 1992.<br>Includes bibliographical references (leaves 191-250).<br>by Andrew Freese.<br>Ph.D.
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16

Vadnal, Jonathan. "Epigenetic Mechanisms in Neurodegenerative Disease." Kent State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=kent1353955013.

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17

Harcombe, Alun Andrew. "Immunological mechanisms in cardiac disease." Thesis, University of Edinburgh, 1995. http://hdl.handle.net/1842/20552.

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The aim of the work presented in this thesis was to examine cell and antibody-mediated immune mechanisms in heart muscle disease. The two conditions studied were acute rejection of cardiac allografts as an example of cell-mediated immune damage, and alcoholic heart muscle disease as a potential example of antibody-mediated disease. In the first study, experiments were performed on 94 endomyocardial biopsies (EMB) from 73 patients to determine the relationship between the ability to grow lymphocytes from EMB in culture and (i) grade of concurrent or future rejections, (ii) the presence of endocardial lymphocytic infiltrates (ELI), and (iii) donor/recipients HLA mismatches. These studies showed that outgrowth of lymphocytes was not closely related to the degree of rejection, not influenced by the use of polyclonal activators in the medium but it was affected by the presence to two HLA mismatches at the DR locus. The presence of ELI was related to rejection but not to outgrowth of the lymphocytes. It was concluded that, contrary to predictions in the literature, the ability to grow lymphocytes from EMB did not indicate presence of impending injection. In the second study, experiments were performed to test the hypothesis that alcoholic heart muscle disease may be caused by autoantibodies to acetaldehyde-modified myocardial proteins. Sera from 61 subjects were tested by Western analysis for antibodies against acetaldehyde-treated human myocardial proteins. No such antibodies were detected in 11 healthy controls subjects, or 28 patients with non-alcoholic heart diseases. In contrast, 4 out of 14 patients with alcoholic heart disease (28%) had detectable antibodies, suggesting a role for these antibodies in alcohol-induced heart muscle disease. To isolate potential antigenic myocardial proteins from small samples of myocardium a technique was developed for rapidly electroeluting proteins separated on a polyacrylamide gel. This system was validated by electroeluting endothelin receptors from human myocardium.
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18

James, V. M. "Molecular insights into the disease mechanisms of startle disease." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1379645/.

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This study describes an in-depth investigation into the pathogenic mechanisms of inherited mutations that lead to disorders of inhibitory glycinergic transmission, primarily the rare human disorder known as startle disease/hyperekplexia. I also investigated mutations causing a similar startle phenotype in cows, mice and zebrafish. Using molecular genetics techniques, I identified pathogenic mutations in the genes that encode for proteins involved in glycinergic neurotransmission, specifically the postsynaptic glycine receptor (GlyR) subunits and the presynaptic glycine transporter GlyT2. Using homology modelling and other computational biology methods, I examined the structural and functional impacts of mutations on protein function, revealing key motifs and amino acids crucial for receptor and transporter activity. Using cDNA cloning and site-directed mutagenesis, I also generated expression constructs for wild-type and mutant proteins that were used in functional tests to measure the impact of pathogenic mutations on glycine receptor and transporter function. For certain animal models of startle disease, I was also able to develop diagnostic PCR tests for pathogenic mutations, which can be used to alleviate further animal suffering by preventing ‘at risk matings’ of carrier animals. Taken together, my findings reveal several new pathogenic mechanisms of GlyR and GlyT2 mutations in startle disease in humans and animals, revealing insights into receptor and transporter function that may be applicable to other neurological disorders.
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19

Weekes, Karen. "Effective coping mechanisms of elite ultra-endurance athletes." Thesis, Ulster University, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648025.

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Background: The compulsion to test one's endurance capacity is widespread in modern society, demonstrated for example by the increased participation rates within adventure sports (Jirasek, 2007). Psychologically based evidence within the corpus reveals that effective coping mechanisms, conducive to elite ultra-endurance athletes performance, is limited. Objectives: The aims of the thesis were four-fold. Firstly, clarification of the stressors elite endurance athletes encounter during their sporting disciplines was sought. Secondly, the study aimed to establish specific, effective coping mechanisms which these athletes implement to overcome stressors. A coping framework was then developed from the information gleaned from the gathered data. Finally, the effectiveness of specific coping mechanisms were illuminated, and the coping framework was tested for accuracy. The overall aim of the thesis is to provide performers and sports psychologists with a comprehensive framework for managing and guiding ultra-endurance based athletes. Method: A mixed methods approach was implemented. A qualitative research approach, guided by grounded theory was employed to contextualize the complexities of elite ultra-endurance athletes coping methods. Semi-structured interviews were conducted with an international cohort of elite, information rich specialists, specifically mountaineers (N=lO) and ultra-distance runners (N=8). Participants also completed the Athletic Skills and Coping Inventory for Sport questionnaire (ASCI-28; Smith et al., 1995). In addition, a case study was adopted to investigate the effectiveness of specific coping tools and test the accuracy of the coping model. Findings: Stressors emerged from personal (e.g., fear), organisational (e.g., social support) and competitive (e.g., opponents) sources, supporting past literature (e.g., Fletcher & Sarkar, 2012). Coping emerged from emotion (e.g., self-talk), approach (e.g., imagery), problem (e.g., goal setting) and appraisal (e.g., self-deception) based approaches. Stressors were linked to specific, effective coping mechanisms, and the benefits of contemporary coping mechanisms, such as mindfulness and meditation, were illuminated. The value of the coping framework for endurance athletes was verified. Recommendations for future research include further exploration into mindfulness as an effective coping mechanism for endurance athletes
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20

Foytik, Elaine Margaret. "Investigating adaptive coping mechanisms in elderly spousal cargivers." CSUSB ScholarWorks, 2001. https://scholarworks.lib.csusb.edu/etd-project/1870.

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This research investigated the coping strategies that elderly caregivers use when caring for a spouse with brain impairment, categorizing their strategies into an external or internal locus of control.
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21

Maness, Natasha Elise, and Kristina Rene Munoz. "Coping Mechanisms Utilized by Single Mothers in College." CSUSB ScholarWorks, 2019. https://scholarworks.lib.csusb.edu/etd/865.

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The purpose of study was to explore the various coping mechanisms used by single mothers who are pursuing higher education. Furthermore, this study examined the various relationships, personal and financial needs the mothers face. This study also explored the interpersonal relationships that exist for single mothers raising their children in the U.S. while facing financial burdens, lack of resources and childcare dilemmas. This study utilized a qualitative design. Data was collected through face-to-face interviews. The data collected from this study will allow for social workers to provide services in order to ensure single mother attending college are utilizing effective coping mechanisms. Furthermore, it will assist social workers and other professional with addressing the needs that single mothers face while trying to get their education and provide for their children simultaneously. It is recommended that colleges and other social service agencies could offer more programs to help assist single mothers with accomplishing their goals. The common themes that were found through this study are: childcare, time management, financial concerns, and support systems. Additionally, themes of coping both adaptive and maladaptive were also recognizable in this study.
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22

Baker, Nita. "Coping with Parkinson's disease in the marital dyad." Thesis, University of Leicester, 1998. http://hdl.handle.net/2381/31166.

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Objectives. The purpose of the current study was to examine how people cope with Parkinson's Disease (P.D.), a chronic and progressive illness, in the context of the marital relationship. More specifically, the study aimed to examine what factors were associated with adjustment in both the people with P.D. and the spouses and to examine the interaction between the partners particularly in respect to congruence in the use of coping strategies. Design. The design was a cross-sectional, correlational design. Method. Twenty-three couples, where one partner was suffering from P.D. participated in the study. Both partners were interviewed separately and completed questionnaires on coping, adjustment and the marital relationship. Results. The adjustment of both partners was related to their husband's/wife's adjustment, to congruence in the use of some coping strategies, to the individual's use of particular coping strategies and to time since diagnosis and stage of disability. There were also relationships between these variables. Conclusion. The interaction between partners is an important factor to consider when attempting to explain adjustment to a chronic illness. If the concept of congruence, with respect to the use of coping strategies, is to be retained then this needs to be clarified and several specific considerations are raised. Further research, of a longitudinal design, is needed to clarify whether the relationships found in the present study are causal and if they are, whether the causality is in one direction or cyclical.
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23

Lau, Hew Mun. "Disease marketing and patient coping : a research study." Thesis, Massachusetts Institute of Technology, 2012. http://hdl.handle.net/1721.1/78159.

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Thesis (S.M.)--Harvard-MIT Program in Health Sciences and Technology, 2012.<br>Cataloged from PDF version of thesis.<br>Includes bibliographical references (p. 80-87).<br>BACKGROUND: There is a high prevalence of disease marketing actions in the United States that are targeted towards patients with chronic illness. However, no study has assessed the direct effects of these marketing actions on patient coping attitudes and behaviors. OBJECTIVES: This study aims to investigate whether the mere presence of disease marketing impacts patient coping and if so, how do they affect patients' coping attitudes and behaviors. METHODS: We conducted a controlled experiment using online questionnaires to assess the disease perceptions, coping decisions and disease disclosure behaviors of 108 subjects. The subjects were divided into two groups where the experimental group (N = 55) was shown marketing actions associated with a fictitious disease called Karlsen's Disease while the control group (N = 53) was not shown any marketing actions. The subjects were then asked a series of questions related to health-related coping behaviors and non-health related social behaviors. T-tests and chi-square analyses were used to analyze the behavioral differences between the experimental (high-marketing) and control (no-marketing) groups. RESULTS: Subjects in the high-marketing group were overall significantly more willing to draft a will than subjects in the no-marketing group (t(106) = 2.64, p = 0.01); High-marketing group subjects were overall significantly more likely to wear a medical ID bracelet than no-marketing group subjects (c²(1, N = 108) = 3.71, p = 0.05); Among subjects who were willing to request a menu accommodation at a dinner party, those who were in the high-marketing group were significantly more likely to disclose their disease to the party host (c²(1, N = 90) = 4.65, p = 0.03); Subjects in the high-marketing group were also significantly more likely to anticipate greater understanding from the party host towards their menu accommodation request. When controlled for gender, women in the high-marketing group were more likely to join a patient support group (t(61) = 1.75, p = 0.09), and less likely to ask family and friends to shave their heads in show of solidarity (t(18) = -1.97, p = 0.07) than women in the no-marketing group; Men in the high-marketing group were more likely than men in the no-marketing group to disclose their health condition to the dinner party host (c²(1, N = 47) = 3.61, p = 0.06). Finally, among subjects with at least a 4-year college degree, those in the high-marketing group were more willing than those in the no-marketing group to wear a face mask to protect themselves from airborne pathogens in crowded public places (t(61) = 1.79, p = 0.08). CONCLUSIONS: Based on our results, the presence of disease marketing is anticipated to have a general positive impact on patient coping attitudes and behaviors. Chronically ill patients exposed to disease marketing actions are expected to anticipate less stigma from others, have increased willingness to disclose their illness and adopt health seeking behaviors. Disease marketing is also expected to have differential impact on patients based on their gender and level of education. Follow-up studies using real patients with chronic illness should be carried out to confirm the findings from this study.<br>by Hew Mun Lau.<br>S.M.
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24

Cvetkovic, ́. Jasmina. "Immune mechanisms in atherosclerotic vascular disease /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-268-X.

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25

Duncan, Lesley Alexandra. "Disease avoidance mechanisms and their implications." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/13155.

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Pathogens and parasites posed significant fitness threats to our ancestors. As a consequence of these enduring threats, there are likely to have evolved a set of cognitive and affective systems designed to facilitate the behavioral avoidance of disease-causing pathogens and their carriers – including individuals who are already infected. The behavioural immune system is a suite of attentional, affective, cognitive, and behavioural responses which function to decrease the probability of contracting pathogens by activating aversive responses to indirect cues that heuristically connote the presence of infectious agents. These cues, however, are at best probabilistically related to the actual presence of pathogens, because the majority of pathogens are too small to be detected. Specific hypotheses were developed to test the influence of pathogen avoidance motivations on three aspects of social cognition. The first focuses on individual variation in concerns with pathogens. The second topic addressed pertains to the types of physical features that act as triggers to activate the behavioural immune system. The third topic addressed the extent to which pathogen avoidance mechanisms play a role in the way we learn cues which connote pathogen presence. In conclusion, this thesis provides evidence which is consistent with the operation of a psychological system which functions to prevent the transmission of infectious threats. The results reported here represent both a substantial contribution to our understanding of the subtle effects of these processes on early cognitive process and a starting point for the application of our existing knowledge to solving real world problems that have great potential for providing social and theoretical rewards.
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26

Sitarz, Kamil Sebastian. "Disease mechanisms in mitochondrial maintenance disorders." Thesis, University of Newcastle Upon Tyne, 2012. http://hdl.handle.net/10443/1679.

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OPA1 and MFN2 are two critical mitochondrial membrane proteins required for mitochondrial fusion. OPA1 mutations account for approximately 60% of cases of autosomal-dominant optic atrophy (DOA) and up to 20% of mutational carriers develop a more severe multi-systemic neurological phenotype (DOA+) in addition to visual failure. MFN2 mutations result in Charcot-Marie-Tooth disease type 2A (CMT-2A) and in a subgroup of patients, the peripheral neuropathy is complicated by optic atrophy, highlighting a degree of phenotypic overlap with DOA+. POLG1 encodes the catalytic subunit of DNA polymerase gamma (POLG) and POLG1- related diseases are clinically highly heterogeneous, ranging from early-onset Alpers- Huttenlocher syndrome to late-onset isolated chronic progressive external ophthalmoplegia. OPA1, MFN2 and POLG1 mutations all result in disturbed mitochondrial DNA (mtDNA) maintenance, with both quantitative (depletion) and qualitative (point mutations and deletions) mtDNA abnormalities having been identified in patient tissue samples. In this PhD project, the disease mechanisms underpinning these nuclear mitochondrial disorders have been studied further. OPA1 and MFN2 mutations were found to result in significant mtDNA proliferation as a likely compensatory mechanism to impaired mitochondrial oxidative phosphorylation. Using a previously-validated repopulation assay, mtDNA replication in cultured POLG1-mutant fibroblasts was severely depressed following a period of ethidium bromide-induced mtDNA depletion. A similar observation was made with OPA1-mutant fibroblasts, but this effect was not as marked as for POLG1-mutant fibroblasts. Significant reorganisation of the mitochondrial network was also apparent for both groups of mutant fibroblasts. Although neuromyelitis optica (NMO) shares some clinical features with DOA, genetic variations within OPA1 are not associated with the risk of developing NMO. Finally, research into DOA and other mitochondrial optic neuropathies have been severely restricted by the lack of the access to retinal ganglion cells (RGCs), precluding direct studies to be performed on the cell type which is preferentially affected in this group of disorders. To circumvent this limitation, human induced pluripotent stem cell (hiPSC) lines have been generated from patient-derived fibroblasts harbouring confirmed OPA1 mutations. The future differentiation of these induced pluripotent stem cell lines into RGCs will hopefully provide a powerful and versatile tool for disease modelling and the development of targeted therapeutic strategies.
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Arsenescu, Razvan I. "NOVEL MECHANISMS IN INFLAMMATORY BOWEL DISEASE." UKnowledge, 2011. http://uknowledge.uky.edu/gradschool_diss/211.

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Inflammatory Bowel Diseases, Crohn's Disease and Ulcerative colitis, are idiopathic chronic conditions with multifactorial determinants. In general, terms, intestinal inflammation results from abnormal host-microbe interactions. Alterations in homeostasis involve host genetic factors, environmental cues and unique luminal microbial niches. We have examined the coordinated expressions of several molecular targets relevant to the mucosal immune system and identified signature biomarkers of IBD. Qualitative and quantitative changes in the composition of microbiota can be related to unique immuno-phenotypes. This in turn can have more systemic effects that involve energy metabolism. Adiponectin, an adipose tissue derived adipokine, can restore cellular ATP levels and fulfills innate immune functions. We have concluded that IBD might represent a state of adiponectin resistance relating to chronic inflammation and obesity status. Lastly we hypothesized that activation of xenobiotic pathway (AHR-aryl hydrocarbon receptor) can further modulate host immune and metabolic responses, and thus contribute to IBD phenotypes. We found that IBD is associated with robust mucosal, aryl hydrocarbon receptor pathway and related to proinflammatory cytokine secretion. We conclude that IBD heterogeneity is reflected through distinct immunophenotypes. Furthermore, environmental cues that involve the AhR receptor and adipose tissue derived adiponectin are important regulators of the inflammatory process in IBD.
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Baddeley, Susan Maureen. "Cellular mechanisms in allergic eye disease." Thesis, University of Southampton, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295267.

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29

Padayachee, Eden Rebecca. "Biochemical mechanisms towards understanding Alzheimer's disease." Thesis, Rhodes University, 2014. http://hdl.handle.net/10962/d1011092.

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The start of the amyloidogenic pathway in Alzheimer’s disease (AD) begins with the deposition of the Aβ₁₋₄₂ peptide surrounded by astrocytes. High levels of arginine and low amounts of neuronal nitric oxide synthase (nNOS) are associated with AD. These astrocytes store reserve arginine that is eventually metabolized by nNOS, within the vicinity of the Aβ₁₋₄₂ peptide. We propose the existence of an association vs. dissociation equilibrium between Aβ and nNOS such that nNOS is an amyloidogenic catalyst for fibrils. When Aβ binds to nNOS, it inhibits the activity of the enzyme (association phase). However when the amyloid peptide dissociates into a form that can no longer bind, later deduced as a fibril, the activity is restored. Thus, the interaction of Aβ with nNOS could serve to regulate the interaction between nNOS and arginine by restoring activity of the enzyme but at the same time promoting fibrillogenesis. Given this event occurring with the neuron, both nNOS and amyloid can serve as a biomarker for the early onset of AD. The enzyme nNOS catalyzed the formation of fibrils in the presence of Aβ peptides, while Ag nps were shown to reverse the fibril formation from Aβ peptides more so than Au and curcumin either through electrostatic or π-π stacking (aromatic) influences. Our studies have shown that the fragments of Aβ₁₋₄₂ i.e. the pentapeptide (Aβ₁₇₋₂₁) and the three glycine zipper peptides (Aβ₂₅₋₂₉, Aβ₂₉₋₃₃, Aβ₃₃₋₃₇) and the full length glycine zipper stretch (Aβ₂₅₋₃₇) all inhibited nNOS activity to varying degrees. The peptides Aβ₁₇₋₂₁ and Aβ₂₉₋₃₃ with their respective Ki values of 5.1 μM and 7.5 μM inhibited the enzyme the most. The Ki values for reversed sequenced peptides (Aβ₁₇₋₂₁r and Aβ₂₉₋₃₃r) were two fold greater than that of the original peptides while the Ki values for the polar forms (Aβ₁₇₋₂₁p and Aβ₂₉₋₃₃p) were between 3-4 fold greater than that of the original peptides. It was also found that Ag nps (Ki = 0.12 μM) inhibited the activity of nNOS the most compared to Au nps; (Ki = 0.15 μM) and curcumin (Ki = 0.25 μM). At 298K, all the ligands bound at a single site on the enzyme (n=1) and a single Trp residue (θ =1), (later identified as Trp678) was made available on the enzyme surface for quenching by the ligands. Increasing the temperature from 298K-313K, increased the value of Ksv and pointed to a dynamic quenching mechanism for Aβ peptides, nps and curcumin interaction with nNOS. The positive signs for entropy and enthalpy for all Aβ peptides nps and curcumin pointed to hydrophobic–hydrophobic interaction with the enzyme. The fact that Kd increased with temperature emphasized the endothermic nature of the binding reaction and the requirement of thermal energy to aid in diffusion of the ligand to the active site. It was concluded that the binding reaction between the ligands and nNOS was non-spontaneous and endothermic at low temperatures (+ΔG) but spontaneous at high temperatures (-ΔG). The two amino acids Tyr706 and Trp678 moved from their original positions, subject to ligand binding. Trp678 moved a minimum distance of 5 Å toward the heme while Tyr706 moved a maximum distance of 14 Å away from the heme. AutoDock 4.2 was a valuable tool in monitoring the distance of Trp678 within the enzyme interior and fluorescence resonance energy transfer (FRET) was efficient in monitoring the distance moved by Trp residues on the enzyme surface.
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Frausto, Karina, and Stephanie Avena. "Master of Social Work Students' Stressors and Coping Mechanisms." CSUSB ScholarWorks, 2017. https://scholarworks.lib.csusb.edu/etd/457.

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The purpose of the present study was to explore and examine the stressors and coping mechanisms used by Master of Social Work (MSW) students. A quantitative survey with some qualitative questions was conducted using a sample of MSW students from California State University, San Bernardino. Data for this study was collected through a self-administered, online questionnaire survey distributed by the MSW program administration. Quantitative data was analyzed through SPSS software by conducting descriptive statistics, frequencies, and independent sample t-test. Qualitative data was analyzed by coding and identifying major themes. Student groups were compared based on program format, which was determined on their standing status as a stipend recipient. The majority of survey participants were non-recipient students (n=45, 60%) and 24 identified as Title IV-E Child Welfare stipend recipients (32%). Results showed that there was no significant difference in the amount of stress experienced by students depending on their program format; however, some differences were identified in preferred coping mechanisms. Based on the results of this study, it is respectfully recommended that the MSW program at California State University, San Bernardino further explores and considers the responses of the students. This study also calls for future research related to MSW students’ stressors and coping mechanisms.
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Yeates, Rebecca. "Coping in young people diagnosed with Inflammatory Bowel Disease." Thesis, University of Sheffield, 2017. http://etheses.whiterose.ac.uk/18037/.

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Volkenant, KristiLynn R. "Children's Coping with Chronic Kidney Disease and Concurrent Adjustment." Bowling Green State University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=bgsu1292689352.

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Alexander, Helen. "Coping with Sickle Cell Disease Using Cognitive Behavior Therapy." ScholarWorks, 2018. https://scholarworks.waldenu.edu/dissertations/5157.

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This project focused on identifying the best evidence available on the use of cognitive behavior therapy (CBT) for pediatric patients and families with sickle cell disease (SCD) to improve their coping skills with pain management. This resulted from an identified gap in nursing practice regarding psychosocial support for this subset of hospitalized pediatric patients. The practice-focused question was whether there was evidence in the literature on the use of CBT techniques to improve parental coping skills with children who have chronic and life-threatening illness that could be utilized with sickle cell disease. The theory of stress and coping guided the underpinnings of the study process. The Johns Hopkins Nursing evidence-based practice model (JHNEBP) was the framework for this project. A systematic review was conducted utilizing research-based articles from the major healthcare databases. The original search resulted in over 12,000 articles. This pool was further refined based upon a link between the pediatric population with chronic or life-threatening conditions and family coping skills. This was further narrowed down based on the use of social-cognitive therapy and coping skills. This process resulted in 6 research articles on the use of CBT with the target population. An evaluation of these studies found evidence that CBT can improve parental coping skills. Nursing support for parental coping with SCD has the positive social impact of decreased parental stress and improved quality of life for both the child and the family unit.
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Spies, Dorothea Janetta. "The coping mechanisms of low-income women : a grounded theory analysis of subjective descriptions of coping." Thesis, Stellenbosch : Stellenbosch University, 2001. http://hdl.handle.net/10019.1/52501.

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Thesis (MA)--University of Stellenbosch, 2001.<br>ENGLISH ABSTRACT: The primary goal of this cross-cultural study was to determine how low-income female farm workers in the Western Cape of South Africa, describe their own coping mechanisms. Eight participants were asked to respond to an open-ended question on how they cope with life's difficulties. The current study formed part of a larger project entitled: "Forgotten women on farms". The psychological distress and resilience of female farm workers of colour in the Western Cape: exploring the possibilities for mental health support (Kruger, 1998). The coping interviews were analyzed by means of grounded theory. Analysis revealed that 28 coping mechanisms were identified by the participants themselves. A distinction was made between problem-focused coping mechanisms and emotion-focused coping mechanisms. Out of the 28 identified mechanisms, 8 were categorized as problem-focused coping mechanisms, while 20 were categorized as emotion-focused coping mechanisms, suggesting that the participants predominantly employ emotion-focused coping mechanisms. It was also found that the emotion-focused coping mechanisms employed by the participants often involved an avoidance of emotion. The findings were discussed by: (i) Critically discussing the way in which emotion-focused coping is traditionally defined within the coping literature. (ii) Comparing this to the conceptualization of the role of emotion by authors of trauma literature. Possible reasons for the prevalent use of emotion-focused coping mechanisms in this particular population were provided. The implications of these findings for assessment of coping strategies and for mental health care in this population were discussed.<br>AFRIKAANSE OPSOMMING: Ole hoofdoeisteiling van hierdie kruis-kulturele studie was om vas te stel hoe laeinkomste vroueplaaswerkers in die Wes-Kaap van Suid-Afrika hulle eie streshanteringsmeganismes beskryf. Agt deelnemers is gevra om op "n oop vraag oor hoe hulle lewensmoeilikhede hanteer, te reageer. Hierdie studie vorm deel van "n groter projek getiteld "Forgotten women on farms". The psychological distress and resilience of female farm workers of colour in the Western Cape: exploring the possibilities for mental health support (Kruger, 1998). Hierdie onderhoude oor streshantering is ontleed m.b.v. "grounded theory". Analise het getoon dat 28 hanteringsmeganismes deur die deelnemers self ge"ldentifiseer is. Onderskeid is gemaak tussen probleem-gerigte hanteringsmeganismes en emosioneel-gerigte hanteringsmeganismes. Uit die 28 gerdentifiseerde meganismes, is 8 gekategoriseer as probleem-gerigte hanteringsmeganismes, terwyl 20 gekategoriseer is as emosioneel-gerigte hanteringsmeganismes, duidend daarop dat deelnemers grootliks van emosioneel-gerigte hanteringsmeganismes gebruik maak. Daar is ook gevind dat die emosioneel-gerigte hanteringmeganismes dikwels "n vermyding van emosie behels het. Hierdie bevindinge is bespreek deur: (i) Die manier waarop emosioneel-gerigte hanteringsmeganismes tradisioneel in die literatuur gedefinieer word krities te bespreek. (ii) "n Vergelyking te tref met die wyse waarop die rol van emosie deur die outeurs van trauma literatuur gekonseptualiseer word. Moontlike redes vir die groter gebruik van emosioneel-gerigte hanteringsmeganismes in hierdie spesifieke populasie is voorsien. Die implikasies van hierdie bevindinge vir die meting van hanteringsmeganismes en vir geestesgesondheidsdienste binne hierdie populasie is bespreek.
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Rutter, Claire. "Illness representation, coping and outcome in irritable bowel syndrome." Thesis, University of Kent, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246600.

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Singhal, Sumeet. "Disease modifiers, mechanisms and monitoring in CADASIL." Thesis, St George's, University of London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418294.

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37

Lim, Andrew Yih-Fan. "Mechanisms of immune regulation in HIV disease." University of Western Australia. School of Surgery and Pathology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0081.

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[Truncated abstract] HIV infection compromises the ability of the host to mount effective immune responses. In untreated HIV disease, immune activation drives high rates of cell turnover and apoptosis, ultimately leading to abnormal and dysregulated cellular function. Immune activation may also induce the expansion of CD4+ regulatory T (Treg) cell populations capable of suppressing anti-HIV responses. Treatment with antiretroviral therapy (ART) allows the recovery of CD4+ T cell numbers in most patients. Persistent deficiencies in the number and function of CD4+ T cells seen in a proportion of individuals may reflect elevated numbers of Treg cells or an imbalanced regulatory-to-effector cytokine milieu. Furthermore, some patients develop paradoxical illnesses associated with the recovery of cellular function, known as immune restoration disease (IRD). The first part of this thesis addresses the role of CD4+ Treg cells in untreated and treated HIV disease. The second part addresses the phenotype of immune cells that express IL-10 and its receptor in untreated and treated patients, and the role of IL-10 in mycobacterial IRD. Firstly, several cell surface markers were evaluated to find a flow cytometry assay that could be used routinely to identify CD4+ Treg cells in HIV-infected patients. I tested CD25, GITR, CTLA-4, NRP-1 and LAG-3, but their expression did not mirror the expression of FoxP3, an intracellular transcription factor specific to CD4+ Treg cells (Chapter 2). Two published studies then described the use of CD127 to identify CD4+FoxP3+ Treg cells in humans. Using CD127, I determined the proportions and numbers of CD4+ Treg cells in untreated HIV-infected patients and in patients in their first year of ART. Proportions of CD4+ Treg cells correlated with the proportions of activated (HLA-DRHI) CD4+ T cells and with plasma HIV RNA levels in untreated patients, but showed an inverse correlation with CD4+ T cell count. In both untreated and treated patients, the proportions and numbers of FoxP3+ cells that expressed CD8 were significantly higher than in uninfected donors. This was clearest in patients with CD4+ T cell counts below 300/'L (Chapter 3). This body of work suggests that the frequencies of CD4+ Treg cells are directly related to the level of HIV-associated immune activation. Phenotyping of FoxP3+CD4+ Treg cells in untreated and treated patients and in uninfected donors revealed that co-expression of CD45RO, CD28, CTLA-4 and markers of activation were similar in all HIV-infected patients and controls. ii FoxP3+CD8+ T cells exhibit lower levels of CD45RO, CD28 and CTLA-4, but higher expression of PD-1 and CD57 (Chapter 4). This suggests that FoxP3+CD8+ T cells may have a reduced functional capacity. It is unclear whether they have regulatory activity by virtue of FoxP3 expression. ... Both patients produced higher levels of IFN? compared with IL-10 in response to mycobacterial antigens. In contrast, patients who experienced uneventful immune reconstitution produced higher levels of IL-10 (Chapter 6). Part 1 of this thesis highlights the importance of using specific cellular markers to identify CD4+ Treg cells, and confirms CD127 as a valuable marker for routine monitoring of blood Treg cells. Part 2 of this thesis demonstrates the important regulatory role of IL-10 in patients receiving ART.
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Urb, Mirjam. "Mechanisms of «Aspergillus fumigatus» chronic airway disease." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=110500.

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Colonization of airways by Aspergillus fumigatus hyphae in immunocompetent patients with chronic lung disease leads to progressive decline in pulmonary function. While a minority of these patients develop a severe allergic response to the fungus, the majority of patients show a decline in lung function and airway hyperreactivity despite the absence of elevated IgE levels, eosinophilia or other evidence of hypersensitivity. Treatment of these non-allergic patients with antifungal drugs improves the symptoms, suggesting that pulmonary complications might be directly caused by A. fumigatus. The mechanisms underlying the acquisition of A. fumigatus colonization and the pathogenesis of pulmonary inflammation have not been studied. Our central hypothesis is that A. fumigatus interacts directly with elements of the immune system to facilitate its own colonization and induces ineffective inflammatory responses that damage host airways. To begin to investigate this hypothesis we used two complementary approaches to examine the interactions of A. fumigatus with elements of the pulmonary immune system. First, we studied the in vitro interactions of A. fumigatus with mast cells, key effector cells involved in orchestrating inflammatory responses and airway reactivity. We found that A. fumigatus triggers mast cell degranulation, while suppressing cytokine expression in an IgE-independent manner. While both degranulation and cytokine transcription required direct contact with mature hyphae, cytokine suppression could also be induced in part by A. fumigatus culture supernatant. Further studies revealed that A. fumigatus hyphae modulated mast cell function by downregulating protein tyrosine phosphorylation and in part by cleavage-dependent activation of protein tyrosine phosphatase 1B (PTP1B). The cleavage of PTP1B was caused by A. fumigatus serine proteases. In parallel, we developed a murine model of A. fumigatus colonization, where airways of healthy mice were colonized with live A. fumigatus by intratracheal injection of conidia embedded within agar beads. Unlike previously described models that induce airway hyperreactivity by repeated challenge with antigen or A. fumigatus spores, infection with this approach resulted in chronic colonization with fungi for up to 28 days. Fungal lesions within the airways were surrounded by a robust neutrophilic inflammation and peribronchial infiltration of lymphocytes. During the first 2 weeks of infection, low level Th2 type responses were seen in the infection, including increased pulmonary IL-4 levels, elevated serum IgE, and a mild increase in airway responsiveness. In addition, significant levels of pro-inflammatory cytokines and chemokines including TNF-α and MIG were observed, suggesting a mixed inflammatory picture. Furthermore, elevated IL-17 levels and presence of RORγ-positive mononuclear cells during late phase of the infection indicated the development of a Th17 response in association with reduction in pulmonary fungal load. Collectively, these results provide insight into the pathogenesis of A. fumigatus-induced chronic airways disease in patients without allergic bronchopulmonary aspergillosis, and suggest a possible role for mast cells in the pathogenesis of this condition.<br>La colonisation des voies respiratoires par les hyphes d'Aspergillus fumigatus chez des patients immunocompétents, mais avec une maladie pulmonaire chronique, entraîne le déclin progressif de la fonction des poumons. Alors qu'une minorité de ces patients développe une réponse allergique aigue au champignon, la majorité montre un déclin dans la fonction des poumons et une hyperréactivité des voies respiratoires malgré l'absence d'une augmentation du niveau des IgE, des éosinophiles ou d'autres indications d'hyper-sensibilité. Le traitement antifongique chez ces patients améliore les symptômes suggérant que le champignon peut être la cause directe des complications observées. Les mécanismes qui sous-tendent la colonisation par A. fumigatus et la pathogenèse de l'inflammation des voies respiratoires restent largement indéterminés. Notre hypothèse centrale stipule que le champignon interagit directement avec des éléments du système immunitaire pour faciliter la colonisation et induire une réponse inflammatoire inefficace qui cause des dégâts aux voies respiratoires de l'hôte. Pour vérifier cette hypothèse, nous avons développé deux approches complémentaires visant à tester l'interaction d'A. fumigatus avec des éléments du système immunitaire pulmonaire. D'abord, nous avons étudié l'interaction in vitro entre A. fumigatus avec les mastocytes, une population clé de cellules impliquées dans la réponse inflammatoire. Nous avons montré que le champignon déclenche la dégranulation des ces cellules, tout en bloquant l'expression des cytokines indépendamment des IgE. Les processus de dégranulation et de transcription des cytokines nécessitent un contact direct avec les hyphes matures, alors que la suppression des cytokines quant à elle peut être induite en partie par le surnageant de culture d'A. fumigatus. Une étude plus approfondie nous a permis de montrer que les hyphes d'A. fumigatus peuvent moduler la fonction des mastocytes via une régulation négative de la phosphorylation d'une protéine tyrosine kinase et, en partie, via l'activation clivage-dépendante de la protéine tyrosine phosphatase 1B (PTP1B). Ce clivage de PTP1B est causé par la serine protéase du champignon. Dans une seconde approche, nous avons développé un modèle murin pour la colonisation par A. fumigatus, où nous avons fait coloniser les voies respiratoires de souris saines avec le champignon par injection intra-trachéale de conidies encapsulées dans des billes en agar. Ce modèle, au contraire des précédents, qui induisent l'hyperréactivité des voies respiratoires par exposition répétée à un antigène ou des spores de A. fumigatus, permet une colonisation chronique par le champignon allant jusqu'à 28 jours. Après ce traitement, les lésions des voies respiratoires, causées par le champignon, se retrouvent entourées par une inflammation neutrophilique robuste ainsi qu'une infiltration péri-bronchiale des lymphocytes. Durant les deux premières semaines qui suivent l'infection, nous avons détecté des niveaux bas d'une réponse type Th2, y compris une augmentation des niveaux des IL-4 pulmonaires, élévation des IgE dans le sérum, et une augmentation légère de la réponse des voies respiratoires. En plus, une augmentation significative des cytokines et des chémokines pro-inflammatoires, y compris les TNF-α et MIG, a été observée suggérant une réponse inflammatoire mixte. Les niveaux élevés des IL-7 et la présence des cellules mononucléaires RORγ-positives durant la phase tardive de l'infection indiquent le développement d'une réponse de type Th-17 associée à une réduction de la charge fongique pulmonaire. Collectivement, ces résultats nous permettent de mieux comprendre le processus de pathogenèse lié aux maladies chroniques des voies respiratoires induites par A. fumigatus chez les patients sans aspergillose bronchopulmonaire allergique, et suggèrent que les mastocytes peuvent jouer un rôle dans cette pathogenèse.
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39

Matthews, Stephen Paul. "Immune mechanisms of respiratory syncytial virus disease." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406348.

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40

Saqlain, Saba. "Investigating Friedreich ataxia disease mechanisms and therapy." Thesis, Brunel University, 2018. http://bura.brunel.ac.uk/handle/2438/15853.

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Friedreich ataxia (FRDA) is an autosomal recessive, neurodegenerative disease caused by the excessive pathological expansion of an unstable GAA trinucleotide repeat within intron 1 of the FXN gene. FRDA occurs due to a pathological GAA repeat ranging from 70-1200 repeats, whereas normal individuals have up to 40 repeats. The prevalence of FRDA in Caucasians is 1:50,000 and it is the most common inherited ataxia. The presence of this large GAA repeat leads to silencing of the FXN gene, resulting in severely diminished levels of the essential mitochondrial protein, frataxin. Frataxin is required throughout development. Therefore, decreased frataxin levels affect the onset and progression of FRDA due to mitochondrial iron accumulation and an increase in oxidative damage, leading to detrimental cellular defects. The pathology of FRDA predominantly affects the cerebellum. Various FRDA cellular and mouse models have been developed to represent the characteristics of this debilitating disease. Data has revealed a positive correlation to exist between an increase in the number of GAA repeats and the severity of the disease. The analysis of these models has shown the expansion of the GAA repeat to be unstable, resulting in both somatic and intergenerational instability. In recent times, a single nucleotide polymorphism (SNP), Asn/Ser46, in the Sirt6 protein of FRDA patients has been associated with a better outcome of the disease. Therefore, Sirt6 heterozygote knockout mice obtained from the Jackson Laboratory were bred with YG8sR FRDA mice, to observe the effects of Sirt6 status on expanded GAA repeat instability, compared to Sirt6 wild type YG8sR FRDA mice. Densitometry analysis showed decreased levels of somatic GAA repeat instability and an increase in FXN protein in 6-month old heterozygous Sirt6 KO mice. However, increased levels of GAA repeat instability and decreased levels of FXN protein was seen in 12-month heterozygous Sirt6 KO mice. The SNP and decreased Sirt6 function may be beneficial to begin with, but not in the long run. A major aim of scientific research is to pave way for the generation of effective therapy. Therefore, attention turned to therapy to increase frataxin protein levels in YG8sR transgenic mice. The effects of the Src kinase inhibitor dasatinib, which had previously been shown to increase frataxin in cell culture, were investigated in YG8sR mice. Dasatinib was administered over a 3-month period, during which time motor coordination ability and frataxin protein levels were investigated. No effect on motor coordination was seen over the course of the treatment. Although, there was a non-significant decrease in frataxin protein levels in the brain in comparison to the vehicle-treated mice. In addition, further analysis by immunohistochemistry showed a decrease of frataxin protein expression in the dorsal root ganglia (DRG). Furthermore, the mean body weight of the dasatinib-treated mice was shown to decrease over time in comparison to vehicle-treated mice. Overall, these studies do not support the use of dasatinib for FRDA therapy. Further studies investigated a new line of GAA repeat expansion-containing FRDA transgenic mice, designated 'YG8LR'. These mice contain approximately 410 GAA repeats, which is significantly more than the previous 'YG8sR' line of mice which contained approximately 220 GAA repeats. As result of this larger GAA repeat, a further decrease of frataxin mRNA and protein was detected in the cerebellum and heart of YG8LR mice compared to YG8sR mice. Further investigations were undertaken to study the epigenetic status and the effects of lowered frataxin protein on the phenotype of the YG8LR model. Increased levels of histone deacetylation and methylation, together with DNA methylation, were detected at the FXN transgenic locus. The YG8LR mice also showed somatic and intergenerational GAA repeat instability as previously detected in earlier FRDA mouse models. Immunohistochemistry analysis of DRG sections showed a decreased level of frataxin protein in YG8LR mice. However, there was an absence of vacuoles in the DRG of the YG8LR mice as previously seen in YG8sR mice, although this particular phenotype is not actually seen in FRDA patients. Motor coordination ability and locomotor activity were significantly decreased as assessed by accelerating rotarod, beam-walk and beam-breaker open-field locomotor analysis. YG8LR mice showed increased glucose intolerance and insulin hypersensitivity in comparison to YG8sR and Y47R mice, investigated by glucose and insulin tolerance tests. Moreover, the most common cause of death in FRDA patients is caused by cardiomyopathy, therefore heart weights were obtained from B6, Y47R, YG8sR and YG8LR mice and a slight increase in mean heart weight was observed in YG8LR mice compared to the other models. This could suggest the lower levels of frataxin leads to the pathology of the heart as seen in FRDA patients. These investigations may help to provide an insight into and confirm molecular mechanisms of the disease, as well as providing a great mouse model for testing future FRDA therapies.
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41

Cross, Rebecca Lee. "Biological mechanisms of depression in chronic disease." Diss., Restricted to subscribing institutions, 2007. http://proquest.umi.com/pqdweb?did=1563274391&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.

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42

Smith, Karen. "Cellular and humoral mechanisms of allergic disease." Thesis, University of Brighton, 2012. https://research.brighton.ac.uk/en/studentTheses/57df8daa-8006-4dff-8d44-ba39572913aa.

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CD 154 is a T cell activation marker, transiently expressed following ligation of the T cell receptor, therefore providing direct access to an antigen-specific T cell population. Using peripheral blood samples taken from allergic individuals and healthy non-atopic controls, this project identified and phenotyped CD 154 + T helper cells following ex vivo stimulation with native allergen extracts (birch pollen, cat dander, grass pollen). Peripheral blood mononuclear cells were stimulated with allergen extract for 16 hours in the presence of Brefeldin A. Responding CD 154 + T cells were identified and phenotyped using multiparametric flow cytometry. Activated CD154+ TH1, TH2 and TRl-Iike cells, that co-expressed IFNy, IL4 and ILIO respectively, were identified in allergic and non-allergic participants. A close correlation was observed between TH1, TH2 and TR1-like cell frequency in non- allergic participants, such that the three parameters increased together to maintain a low TH2:TH1 ratio. The relationship between TH1, TH2 and TR1-like responses was dysregulated in allergic individuals, with abrogation of the IL10 response and a higher TH2:THI ratio. A close correlation was observed between Th2 cell frequency and the absolute concentration of birch-specific IgE. This work confirms previous reports of a more differentiated T cell phenotype in allergic subjects with regard to seasonal allergens. The detection of CD154+ T cells after short-term antigen stimulation may be a useful method for the detection of T cell responses to allergens when cost, speed and convenience are priorities. The CD 154 assay was also used to investigate allergen-specific T cells in two situations: [1] during allergoid immunotherapy and [2] at peak pollen season compared to out of season. This preliminary data suggests an increased frequency of TH2 cells in allergic individuals during the birch pollen season compared to healthy non-allergic controls, and a decrease in the TH2:THI ratio following successful immunotherapy. A proliferation assay utilising the cell surface PKH dye was also optimised to investigate proliferative responses to native allergen extracts in allergic and non- allergic subjects. Colonisation with superantigen-producing staphylococci is common in atopic diseases and may contribute to the initiation and maintenance of allergic sensitisation. However, little is known regarding T cell responses to superantigens in atopic individuals. This project sought to investigate T helper cell responses to the superantigen Staphylococcal Enterotoxin B (SEB) from Staphylococcus aureus in non-atopic individuals and highly atopic polysensitised individuals. Peripheral blood mononuclear cells were stimulated with SEB for 16 hours in the presence of Brefeldin A. Responding TH1, TH2, TH17, TR1-like and naturally occurring regulatory T cells were identified using multiparametric flow cytometry. This preliminary study identified a downregulated T H 17 response to the superantigen SEB in highly atopic individuals that does not relate to T Reg cell frequency or TCRVP3 expression. The Pollen-Food Syndrome (PFS) is caused by sensitisation to homologous panallergens within aeroallergens and food proteins. Information regarding the sensitisation profiles of individuals with PFS in the UK is limited and investigations into causative panallergens are not routinely performed. In a small study, patients with symptoms suggestive of PFS were recruited. from the Allergy Clinic at Brighton and Sussex University Hospital NHS trust. A standardised food allergy questionnaire was completed and serum analysed by component-resolved diagnosis using ImmunoCAP ISAC technology. This study cohort conformed to the Northern European pattern of birch-pollen associated PFS with cross-reactivity between the major birch pollen allergen Bet v 1 and homologues in food proteins. Sensitisation to LTPs and profilins was also noted, but the clinical relevance of these remains to be elucidated. Profilin sensitisation was associated with reactions to a significantly larger number of foods compared to PR-10 mono sensitised individuals.
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43

Aman, Yahyah. "Investigating mechanisms of pain in Alzheimer's disease." Thesis, King's College London (University of London), 2018. https://kclpure.kcl.ac.uk/portal/en/theses/investigating-mechanisms-of-pain-in-alzheimers-disease(2bbc4948-3804-4e23-baa3-cddb8b4a6321).html.

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Experience of pain is a key contributor to challenge of care in Alzheimer’s disease (AD) individuals and is often associated with age-related medical comorbidities, commonly musculoskeletal conditions such as osteoarthritis (OA). Significant alteration in perception of pain is an important clinical issue in patients with AD and its effective treatment is increasingly recognised as a critical unmet clinical need. Currently, management of pain has been hindered by difficulties in the assessment of pain partly due to the impaired ability to communicate sensations as well as the inadequate understanding of the underlying mechanisms of pain in this susceptible patient group. Animal models of AD recapitulate many of the clinical and pathological features of the human AD and thereby offer to be a powerful tool in order to delineate mechanisms in AD. This thesis aims to investigate possible alterations of nociceptive sensitivity, in acute and chronic pain models, using the transgenic double-mutant APPswe×PS1.M146V (TASTPM) mouse model of AD. Furthermore, it aims to elucidate the associated plastic changes along the pain pathway (i.e. spinal cord and thalamus) of the preclinical TASTPM model and evaluate its translational implication using human post-mortem tissue obtained from AD patients with chronic pain conditions. This thesis provides preclinical evidence for alterations in nocifensive behaviour that are associated with dysfunction of the opioidergic system in TASTPM mice compared to age- and gender-matched wild-type (WT) controls. Specifically, TASTPM mice display reduced sensitivity to acute noxious thermal stimulation and impaired persistent pain-like behaviour in a model of OA induced by an intra-articular administration of monosodium iodoacetate (MIA). These changes coincide with impairment of cognition, development of amyloid plaques in the brain, and intraneuronal accumulation of amyloid precursor protein/β-amyloid (APP/Aβ) in the spinal cord of TASTPM mice. Increase in expression of endogenous inhibitory peptides: enkephalins in the dorsal horn and β-endorphins in plasma correlate with the attenuated nociceptive sensitivity to noxious thermal stimulation and persistent pain, respectively, in TASTPM mice. Administration of naloxone, an opioid antagonist, re-establishes normal sensory thermal thresholds and unmasks the reduced MIA-induced mechanical allodynia exhibited by the TASTPM mice. Subsequent administration of the analgesic morphine, an opioid agonist, induces heightened responsiveness in the TASTPM mice compared to WT controls. Together, these findings implicate the disruption of the opioidergic system as a common mechanism underlying the reduced acute nocifensive and impaired persistent pain-like behaviour in TASTPM model of AD. In parallel to these observations, alteration in the neuro-immune plasticity along the pain pathway is also identified as a possible mechanism that underlies impaired persistent pain-like behaviour exhibited by AD mice. In particular, diminished spinal microgliosis in response MIA administration in the periphery coupled to inability of gabapentin to induce analgesia were evident in TASTPM. These data indicate blunted central sensitisation in the model of AD. Intriguingly, increase in the extent of neuroinflammation is observed in the thalamus of TASTPM mice compared to WT, in the model of OA. However, no change in APP/Aβ pathology was detected in both the spinal cord and brain of TASTPM mice. Analyses of human post-mortem tissue obtained from AD individuals lend support to preclinical observations in TASTPM mice of intraneuronal accumulation of APP/Aβ and amyloid plaque deposition in the spinal cord. The other pathological hallmark of AD, neurofibrillary tangles (NFT), was not detected in the spinal cord of AD patients. Assessment of supraspinal structures involved in pain processing, including the thalamus, reveal presence of both amyloid plaques and NFT, which increased in abundance with progression of AD. Moreover, evaluation of AD-associated pathology in AD individuals with a clinical history of chronic pain and/or persistent analgesic use displays no alteration in deposition of amyloid plaques and NFT. However, increase in microglial activation was observed in both the spinal cord and supraspinal regions compared to AD subjects with no clinical pain record. These data provide additional support for the exacerbation of ongoing neuroinflammation identified in the preclinical TASTPM mice in a model of OA. Such observations from human post-mortem tissue reinforce the advantage of utilising the TASTPM model of AD in order to delineate mechanisms of pain in AD as it recapitulates some of the key features that are observed in human AD patients. Taken together, the findings of this thesis have important clinical implications for the care of patients with AD who have deteriorating cognitive function along with reduced sensitivity to pain. Altered pain sensitivity could be considered in assessing clinical risk as it may be associated with neuropsychiatric symptoms as well as an increased risk of injury during daily routine activities. Finally, these data highlight the need to re-evaluate current treatments, such as opioids, or develop novel therapeutic strategies for management of pain in individuals with AD.
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44

Köchert, Karl. "From high-dimensional data to disease mechanisms." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2011. http://dx.doi.org/10.18452/16297.

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Die aberrante Aktivierung des NOTCH Signalweges trägt entscheidend zu verschiedensten malignen Erkrankungen im Menschen bei. Basierend auf der Analyse von hochdimensionalen Microarray-Datensätzen von klassischen Hodgkin Lymphoma Fällen und nicht-Hodgkin Fällen, haben wir eine Hodgkin Lymphoma-spezifische NOTCH Signatur identifiziert. Diese wird von dem essentiellen NOTCH-Koaktivator Mastermindlike 2 (MAML2) signifikant dominiert. Auf der Grundlage dieses Resultates haben wir die Rolle von MAML2 im Kontext des Hodgkin Lymphoma-spezifischen, aberrant regulierten NOTCH Signalweges weiter untersucht. Die signifikante Überexpression von MAML2 im Hodgkin Lymphom konnte in verschiedenen Hodgkin Lymphom Zelllinien und auch durch die immunhistochemische Analyse von primären Hodgkin Lymphom Fällen verifiziert werden. Mit Hilfe des Knockdowns von MAML2 bzw. der Inhibition des NOTCH Signalweges durch die Verwendung einer kompetitiv, dominant-negativ wirkenden, trunkierten Variante von MAML1 konnte daraufhin gezeigt werden, dass die Überexpression von MAML2 der limitierende Faktor für die Hodgkin Lymphomaspezifische, pathologische Deregulation des NOTCH Signalweges ist. Die MAML2- vermittelte Überaktivierung des NOTCH Signalweges ist darüber hinaus essentiell für die Proliferation von Hodgkin Lymphom Zelllinien und die aberrante Expression der NOTCH Zielgene HES7 und HEY1. Das konstitutive Vorhandensein von aktiviertem, intrazellulären NOTCH1 in Hodgkin Lymphom Zelllinien impliziert darüber hinaus,dass der Signalweg im Hodgkin Lymphom zellautonom aktiviert ist. In dieser Arbeit wird damit ein neuer, pathologisch hochwirksamer Mechanismus der NOTCH Signalweg-Deregulation aufgedeckt.<br>Inappropriate activation of the NOTCH signaling pathway, e.g. by activating mutations, contributes to the pathogenesis of various human malignancies. Using a bottom up approach based on the acquisition of high–dimensional microarray data of classical Hodgkin lymphoma (cHL) and non-Hodgkin B cell lymphomas as control, we identify a cHL specific NOTCH gene-expression signature dominated by the NOTCH co-activator Mastermind-like 2 (MAML2). This set the basis for demonstrating that aberrant expression of the essential NOTCH co-activator MAML2 provides an alternative mechanism to activate NOTCH signaling in human lymphoma cells. Using immunohistochemistry we detected high-level MAML2 expression in several B cell-derived lymphoma types, including cHL cells, whereas in normal B cells no staining for MAML2 was detectable. Inhibition of MAML protein activity by a dominant negative form of MAML or by shRNAs targeting MAML2 in cHL cells resulted in down-regulation of the NOTCH target genes HES7 and HEY1, which we identified as overexpressed in cHL cells, and in reduced proliferation. In order to target the NOTCH transcriptional complex directly we developed short peptide constructs that competitively inhibit NOTCH dependent transcriptional activity as demonstrated by NOTCH reporter assays and EMSA analyses. We conclude that NOTCH signaling is aberrantly activated in a cell autonomous manner in cHL. This is mediated by high-level expression of the essential NOTCH coactivator MAML2, a protein that is only weakly expressed in B cells from healthy donors. Using short peptide constructs we moreover show, that this approach is promising in regard to the development of NOTCH pathway inhibitors that will also work in NOTCH associated malignancies that are resistant to -secretase inhibition.
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45

Graziano, Adriana Carol Eleonora. "Molecular mechanisms involved in krabbe s disease." Doctoral thesis, Università di Catania, 2014. http://hdl.handle.net/10761/1507.

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Krabbe disease is an autosomal recessive disorder resulting in the deficiency of galactosilcerebrosidase (GALC), a lysosomal enzyme involved in the catabolism of two lipids extremely represented during formation of myelin sheet: galactosylceramide and psychosine. Despite the GALC activity deficiency, galactosylceramide does not increase in the brain of patients, while psychosine accumulation is reported as cause of myelin-generating cells death and of severe neurodegeneration. The present work outlined a molecular explanation for how psychosine mediates a dose-dependent cell death in oligodendrocytes precursor and fibroblast cells with and without GALC mutation. In addition, it was analyzed how this mechanism may interfere in oligodendrocytes maturation. The connexins play essential roles in cell homeostasis, growth, differentiation and death. Among connexin family members, Connexin43 is recently reported as an active element in apoptosis by gap junction-dependent or -independent mechanisms. Still today, there are no scientific researches evaluating Connexin43 expression and localization in normal and in GALC mutated oligodendrocytes precursor cells. The results of this study established that the different effects of exogenous psychosine addition could be linked to different sensitivity of cell membrane. Furthermore, it was determined a primary involvement of cell proliferation and a relationship between caspase-3 activation and disturbance of membrane-activated protein involved in cellular growth and survival. Psychosine treatments resulted in proteolysis of procaspase-3 proportioned to PTEN up-expression and PI3K activity down-regulation, confirmed by Bad release, p53 enhanced levels and decrease of NF-kB. The intrinsic apoptosis activation was established. Moreover, psychosine treated oligodendrocyte precursors increased Connexin43, demonstrating preferential intracytoplasmatic localization and indicating that no gap- junction was involved. These in vitro findings were supported by examination of Connexin 43 levels in mouse brains: wild-type mouse brain proteins were compared to those ones of twitcher mouse, a natural occurring model of Krabbe disease. Reminding that Connexin43 never was found in mature oligodendrocytes, the second part of this work was pioneer in evaluating Connexin43 expression during wild-type- and GALC-mutated oligodendrocytes maturation steps without psychosine treatment. In experimental condition applied, it was verified that wild-type oligodendrocyte progenitors differentiate into a mature phenotype with loss of Connexin43. Under the same condition, GALC-mutated oligodendrocyte precursor did not express marker of maturity, they became multinuclear and Connexin43 levels remained higher than control, suggesting that psychosine is accumulating in early steps of oligodendrocyte precursor cell maturation. Taken together, these findings led to the general idea that psychosine may functionally impact cells through interference on the growth system and alteration in maturation programme, strongly related to Connexin 43 expression. Thus, the third part of this work probed the likelihood of using adipose tissue-derived mesenchymal stem cells (AT-MSCs) as source of oligodendrocytes. Two different conditioned media were used and the results demonstrated that AT-MSCs can be influenced by the environment versus a neural phenotype. For this reason, stem cells can furnish potential material for cell replacement therapy. In summary, this thesis provides a new and unexplored molecular-mechanism for understanding the appearance and maintaining Krabbe disease hallmark. This work is the first description of a potential Connexin43 involvement in oligodendrocytes maturation and psychosine-inducted toxicity.
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46

Malan, Leoné. "Cardiovascular dysfunction and specific coping mechanisms in Africans / L. Malan." Thesis, North-West University, 2005. http://hdl.handle.net/10394/767.

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Motivation: Cardiovascular dysfunction and hypertension are some of the leading causes of morbidity and mortality in the African population. According to the World Health Organisation the increases in these diseases are escalating in developing countries. Apart from the contributory role of genetics towards the incidence of hypertension, evidence regarding lifestyle as a determinant or marker of cardiovascular diseases in this group is not well known. The interaction of psychological and physiological mechanisms can contribute towards a broader scope of behavioural physiology in the higher prevalence of hypertension in Africans. Objectives: The main objective of the research in this thesis was to compare specific coping mechanisms of Africans with regard to cardiovascular dysfunction. Methodology: Manuscripts presented in Chapters 3, 4, and 5 made use of the cross-sectional comparative epidemiological "Transition and Health during Urbanisation in South Africa" (THUSA) project. The subjects included apparently healthy African men and women, which were recruited as a convenience sample from the North West Province, South Africa. Anthropometric measurements were taken and demographic questionnaires completed. An adapted Setswana COPE questionnaire was used to classify men and women as predominantly active (AC) or passive (PC) in coping style. Subjects were further subdivided into rural and urban groups (Manuscript Two), as well as younger (≤ 40) and older (≥ 45) age groups (Manuscript Three). The General Health Questionnaire (GHQ) was used to measure subjective perception of health in all three manuscripts. Blood pressure was recorded continuously before and during application of the handgrip test using the Finapres apparatus. Subjects were classified as normotensive and hypertensive after blood pressure measurement by the Finapres and the Riva-Rocci/Korotkoff method. The emphasis in this study was on the cardiovascular reactivity values. Fasting, resting serum renin activity, cortisol, prolactin, testosterone, high density lipoprotein, triglycerides, glucose and plasma fibrinogen values were correlated with cardiovascular and psychological variables. Significant differences between variables were determined by means of variance analyses (Manuscript One and Two adjusted for age; Manuscripts One, Two and Three adjusted for resting cardiovascular data). A logistic regression analysis was performed to determine the most significant determinants of urbanisation. All THUSA subjects and parents of under-aged adolescents gave informed consent and the study - was approved by the Ethics Committee of the Potchefstroom University for Christian Higher Education. The reader is referred to the abstracts at the beginning of each separate manuscript in Chapters 3 - 5 for a description of the subjects, study design and analytical methods used in each paper. Results and conclusions of the individual manuscripts: Results from the THUSA study showed that PC men and women reported more symptoms typical of an abnormal psychological and physiological profile than AC men and women. The PC men, compared to AC men, exhibited a larger vascular reactivity response as well as larger plasma renin activity. In contrast, the AC women showed a larger non-significant vascular reactivity response than PC women. All subjects though reacted with increased vascular reactivity on the stressor. Men with a PC strategy showed enhanced vascular reactivity, a perception of poorer health and larger stressor plasma renin activity. PC women reported more depressive symptoms and younger PC women indicated a higher prevalence of hypertension than younger AC women. As a follow-up on the first manuscript, the aim was focused mainly on including the environmental effect, namely urbanisation, as possible explanatory factor for the atypical physiological AC women’s' coping style. The rural AC subjects indicated more typical active coping central cardiac responses than rural PC subjects whereas urbanised AC and PC subjects indicated greater peripheral responses and hypertension prevalence rates. In addition, the urbanised AC men and women and PC women as opposed to their rural counterparts indicated symptoms more of a distress situation with increased values of prolactin and decreased values of testosterone. This was also accompanied by a perception of poorer health in women. Results of the AC style suggests that the typical physiological AC stimulation pattern of urbanised subjects and especially the women is dissociated from the "normal" physiological AC reaction and is now exhibited as a typical PC physiological stimulation pattern. The greater vascular reactivity, hypertension prevalence, perception of poorer health and endocrine distressed profile are associated with a PC and dissociated physiological AC style in an urban context in African men and women. No differences with regard to resting blood pressure or endocrine values were obtained when the AC and PC urbanised groups were compared. Africans develop cardiovascular dysfunction/hypertension during chronic stress or urbanisation. This implies a dissociation/habituation of physiological systems of African men and women despite having an active coping strategy. Active coping is, therefore, not necessarily "successful". Results of the first two manuscripts direct further investigation concerning the effects of ageing and urbanisation on the development of cardiovascular dysfunction and metabolic syndrome indicators in gender groups. The second manuscript showed that all rural AC subjects exhibit a more typical active coping central cardiac response and that rural PC and all urbanised subjects (AC and PC) exhibit enhanced peripheral vascular responses on the - handgrip test. Where peripheral vascular responses were more expected from older individuals in Manuscript Three, the occurrence of this pattern is strengthened in the younger subjects. The greater fibrinogen values in all younger urbanised women (AC and PC) compared to rural women further strengthen the risk for the development of cardiovascular disease. Increased vascular reactivity, abdominal obesity and increased levels of triglycerides as well as perception of poorer health were apparent in the urbanised AC women, PC men and women in comparison to their rural counterparts. The typical physiological AC stimulation pattern of urbanised women is dissociated from the "normal" physiological AC responses and is now exhibited as a typical PC physiological stimulation pattern. A typical PC style in older urbanised subjects is implicated in the greater hypertension prevalence. To conclude, it seems as if young urbanised Africans, and especially women, exhibit an AC style behaviourally with a dissociated physiological AC reaction pattern. Physiologically these women resemble a typical PC physiological cardiovascular and endocrine profile. This typical PC cardiovascular stimulation pattern is strengthened by a distressed endocrine profile, significant metabolic syndrome indicators and a 'perception of poorer health. Older PC style subjects also presented a greater hypertension prevalence. In this study it seems that cardiovascular changes that appear at a younger age might be influenced by other factors including urbanisation as a lifestyle factor as well as specific coping styles. Finally, a careful suggestion is made that specific coping mechanisms could be seen as a possible risk marker in the development of the metabolic syndrome.<br>Thesis (Ph.D. (Physiology))--North-West University, Potchefstroom Campus, 2005.
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47

George, Catherine Louise. "Trauma, attachment, emotion regulation and coping mechanisms in mental health." Thesis, University of East Anglia, 2018. https://ueaeprints.uea.ac.uk/68933/.

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A significant proportion of the population experience adverse events in childhood. For some, the literature demonstrates that these adverse events contribute towards the later development of severe and enduring mental health problems such as psychosis and borderline personality disorder (BPD). These diagnoses are associated with poor outcomes including reduced Quality of Life (QoL). Whilst we are making progress in our understanding though the advances in theoretical models, reviews of current literature, and new research, the multi-faceted mechanisms and influence of different variables require further exploration. The first aim of this research was to ascertain if coping mechanisms were related to QoL in individuals diagnosed with schizophrenia. The second aim was to explore whether BPD, psychosis and control populations differ in their trauma history, symptomatology (psychotic and BPD), attachment style and difficulties in emotion regulation; to assess if trauma type and severity relate to symptomatology, attachment and emotion regulation; and finally, to assess if attachment or emotion regulation influence the relationship between trauma and symptomatology. A systematic review of the literature generated 2795 studies. Nine studies met inclusion criteria for data synthesis. A quantitative questionnaire-based empirical study involved 120 adult participants (28 BPD, 29 psychoses and 63 controls). Synthesis demonstrated evidence for a small to medium positive correlation between problem-focused coping and QoL. Between group differences were found for all variables and trauma correlated with all variables. Only emotion regulation mediated the influence of trauma on both BPD and psychotic symptomatology. More research is required for conclusions to be determined about how coping relates to QoL in schizophrenia. The empirical results evidence the necessity of further research and development towards multifactorial models which incorporate the complex interacting influences of trauma, attachment and emotion regulation. Models should be integrative and be applied beyond diagnostic boundaries to best promote recovery.
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48

Kempen, Sarah. "Depression, Burnout, Coping Mechanisms and Resilience amongst Temmincks Pangolin Conservationists." Diss., University of Pretoria, 2020. http://hdl.handle.net/2263/78515.

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Temmincks pangolins are the world’s most trafficked mammal. This animal is unique to Southern Africa, and just as rare are the conservationists who are working against all odds to save this species from extinction. While the incidence of poaching within South Africa is increasing, as is the value of a pangolin, the conservation workspace is rapidly becoming increasingly dangerous. In light of the above, one cannot help but be concerned for the well-being of the pangolin conservationists. Despite engaging in meaningful work, the conservationists are exposing themselves to prolonged stress that is likely to impact their well-being. The purpose of this study is to explore the well-being of Temmincks pangolin conservationists in terms of state and trait depression as well as burnout. Furthermore, the study aims to understand whether coping mechanisms or resilience mitigate the effect of the potential depression and burnout. Therefore, a sequential explanatory mixed-method design was adopted for this study. The quantitative data was gathered using the Maslach Burnout Inventory General Survey (MBI-GS), the State Trait Personality Inventory Form Y (STPI-Y) depression subscale, the Coping Orientations to Problems Experienced (COPE) questionnaire and the Predictive 6 Factor Resilience Scale (PR6). The qualitative data was collected utilising a semi-structured interview. Results indicated that the participants were currently experiencing both state and trait depression. Additionally, a third of the sample is at risk of developing burnout. In spite of this, the participants displayed the presence of goal focus, tenacity and collaborative spirit. These elements of resilience were shown to assist the conservationists to persist through adversity. The participants also showed the use of effective coping mechanisms, namely; accepting, planning and critically engaging with perceived stressors. These coping mechanisms were shown to enhance the presence of the resilience indicators. Thus, despite depression and burnout impacting negatively on their well-being, the participants are utilising coping mechanisms and resilience which enhances their well-being. Recommendations included a developmental workshop focusing on fostering effective coping mechanisms to build stronger resilience and ward off potential burnout and possibly ameliorate current depression experiences.<br>Dissertation (MA (Psychology))--University of Pretoria, 2020.<br>Psychology<br>MA (Psychology)<br>Unrestricted
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49

Hawk, Nita C. "The implication of stress and coping mechanisms in the superintendency." Diss., Columbia, Mo. : University of Missouri-Columbia, 2008. http://hdl.handle.net/10355/5564.

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Thesis (Ed. D.)--University of Missouri-Columbia, 2008.<br>The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on June 8, 2009) Vita. Includes bibliographical references.
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50

Beadle, Nina Elizabeth. "Mitochondrial DNA defects and human disease : the molecular mechanisms underlying disease expression." Thesis, University of Newcastle Upon Tyne, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.544209.

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