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1
Williams, Julie M. "Coping with asthma : investigation and intervention using the self-regulation model." Thesis, University of St Andrews, 1995. http://hdl.handle.net/10023/2800.
Testo completoAbstract (sommario):
The Self-Regulation Model (Leventhal, Nerenz & Steele, 1984) highlights the roles of patients' illness representations, coping, emotional reactions and appraisal of coping in the progression of chronic disease. This thesis incorporates previous literature on adherence, panic-fear and selfmanagement interventions into the model in order to (a) investigate coping with asthma and (b) develop an intervention aimed at improving asthmatic control. New measures of asthmatic control and illness representations of the consequences of having asthma were developed in order to operationalise the model. A cross-sectional study investigated factors influencing asthmatic control in a sample of 35 adult asthma sufferers recruited through a single general practice. Coping was poor, adherence being low and less than 50% of participants reporting current Peak Flow monitoring or medical contact during the previous 12 months. Good coping appeared to be a response to poor asthmatic control, rather than prophylactic. Good asthmatic control was associated with low perceived consequences, recent medical contact, moderate panic-fear and low general avoidance coping. These results imply that asthmatic control may be improved by encouraging sufferers to maintain regular contact with outpatient services and to implement prophylactic coping. Since epidemiological and clinical evidence suggested asthmatic control to be poor in young adults, an intervention was developed to improve asthmatic control in this group by modifying illness representations, coping and panic-fear. The intervention was evaluated in a randomised controlled study of 50 student asthma sufferers identified initially through an epidemiological screening of 2,979 students. It led to increased Preventer medication use and Peak Flow monitoring and decreased distress over the condition. However, the coping process changed and asthmatic control improved even in the control group, perhaps because self-monitoring of asthmatic control for the study constituted a change in coping. This unanticipated result was entirely compatible with the Self-Regulation Model. The thesis dearly demonstrates value of the Self-Regulation Model in understanding asthma self-management and developing clinical interventions.
2
Ollé, Monge Marta. "Novel insights in occupational asthma due to persulfate salts." Doctoral thesis, Universitat Autònoma de Barcelona, 2016. http://hdl.handle.net/10803/399518.
Testo completoAbstract (sommario):
El asma relacionada con el trabajo se define como el asma causada por la exposición a agentes que se encuentran en el lugar de trabajo, y es responsable de hasta un 25% de los casos de asma de inicio en la edad adulta. En los países industrializados es una de las causas más comunes de enfermedad respiratoria ocupacional. Concretamente, el asma ocupacional (AO) se atribuye a exposiciones en un particular ambiente ocupacional y no a estímulos fuera del lugar de trabajo, y puede estar inducido tanto por la sensibilización a un agente específico (AO inmunológico) como por exposición a sustancias irritantes (AO no inmunológico). Se han descrito más de 400 agentes causantes de AO y se dividen en agentes biológicos de alto peso molecular (APM) como proteínas, glicoproteínas y polisacáridos, y agentes químicos de bajo peso molecular (BPM) como sustancias químicas sintéticas, compuestos naturales, fármacos y metales. Las sales de persulfato son agentes químicos de BPM presentes en los productos decolorantes del cabello a concentraciones superiores al 60%. Estas sustancias son capaces de producir una sensibilización inmunológica y posterior enfermedad alérgica (dermatitis de contacto y asma bronquial), y son reconocidas como la principal causa de AO entre los profesionales de peluquería. Sin embargo, los detalles de la respuesta inmune implicada en el AO inducido por sales de persulfato no son bien conocidos, ya que parecen diferir de la respuesta típicamente alérgica de tipo 2. En algunos casos, se ha propuesto un mecanismo inmunológico mediado por inmunoglobulina-E (IgE) a pesar de las evidencias de una respuesta inmune tipo 1. En este sentido, un modelo murino de asma inducido por sales de persulfato, previamente validado, ha permitido ampliar el conocimiento de la fisiopatología implicada en este tipo de AO.
La primera parte de la presente tesis se centra en el estudio de la persistencia de la respuesta asmática a sales de persulfato tras la sensibilización dérmica y tras una inhalación intranasal de persulfato amónico en ratones sensibilizados. Estos estudios mostraron una progresiva disminución de la respuesta asmática con el tiempo y los síntomas asmáticos llegaron incluso a desparecer, de forma parecida a lo que puede ocurrir en los pacientes con AO cuando cesa la exposición al agente causal. Sin embargo, no está claro que la completa eliminación de la exposición al agente sensibilizante sea la medida más eficiente ya que muchos pacientes permanecen sintomáticos. En este sentido, los ratones sensibilizados mostraron signos de sensibilización sistémica a largo plazo que les haría susceptibles a desarrollar una nueva respuesta asmática en el caso de una posible re-exposición al agente causal.
El objetivo de la segunda parte de la tesis es evaluar el papel de la IgE y los mecanismos implicados en el desarrollo de la respuesta inmune en el AO causado por agentes de BPM, ya que el rol que desarrolla la IgE en este tipo de asma no está bien dilucidado. Mediante el bloqueo de la IgE, se pudieron estudiar los efectos del tratamiento con el anticuerpo monoclonal (AcM) anti-IgE en el modelo murino de AO inducido por sales de persulfato. La administración del AcM anti-IgE neutralizó completamente los niveles de IgE en suero y mejoró los síntomas asmáticos como la hiperrespuesta bronquial y los parámetros inflamatorios. Estos hallazgos sugieren la implicación de un mecanismo inmunológico donde la IgE puede tener un papel relevante para la fisiopatología del asma causada por agentes de BPM.
En conclusión, los estudios de esta tesis arrojan conocimientos en la fisiopatología del AO a sales de persulfato y proponen una compleja interacción entre la respuesta inmune innata y una respuesta adaptativa mixta tipo1-tipo2.<br>The exposure to specific agents present in the workplace is thought to account for up to 25% of all cases of adult-onset asthma leading to work-related asthma, which is a common cause of work-related lung disease in the industrial world. Specifically, occupational asthma (OA) is attributable to exposure in a particular work environment and not to stimuli outside the workplace, induced by either sensitization to a specific substance (sensitizer-induced OA) or by exposure to an inhaled irritant at work (irritant-induced OA). More than 400 agents are reported to cause OA. They can be divided into biological agents of high molecular weight (HMW) (>5 KDa), such as proteins, glycoproteins and polysaccharides, and chemical agents of low molecular weight (LMW) (< 5 KDa) such as synthetic chemicals, natural compounds, drugs and metals. Persulfate salts are LMW chemical compounds present in hair bleaching products at concentrations up to 60%. They are capable of causing immunological sensitization and subsequent allergic disease (such as contact dermatitis and bronchial asthma), and are the main cause of OA among hairdressers. Nevertheless, no consensus has been reached regarding the details of the immune response involved in persulfate-induced OA, as it seems to differ from the typical allergic type2 immune response. In some cases, an IgE-mediated mechanism has been proposed despite evidence of a type 1 immune response. In this connection, a validated mouse model of persulfate-induced asthma has provided valuable knowledge about the physiopathology involved in this type of OA.
The first part of this thesis focuses on the study of the persistence of the asthmatic response to persulfate salts after dermal sensitization (Chapter 1) and after specific persulfate challenge in sensitized mice (Chapter 2) in the mouse model of persulfate-induced asthma. These studies showed a progressive decrease in the asthmatic response over time and even found that the asthma symptoms may disappear, perhaps mirroring what happens in patients when the exposure to the causal agent ceases. Nevertheless, it is not clear that complete removal from the exposure to the sensitizing agent is the most efficient therapeutic approach, as many patients remain symptomatic despite avoidance of the causal agent. In this context, sensitized mice exhibited signs of long-term sensitization which would make them susceptible to developing a new asthmatic response when re-exposed to the sensitizing agent.
The aim of the second part of this thesis was to explore the role of IgE and the mechanisms involved in the development of the immune response in this type of OA due to LMW agents. By neutralizing the IgE, we wanted to study the effects of anti-IgE monoclonal antibody (mAb) treatment in the established mouse model of persulfate-induced OA (Chapter 3). The administration of anti-IgE mAb completely neutralized serum IgE and improved asthma symptoms such as airway hyperresponsiveness (AHR) and inflammation patterns in the mouse model of OA, suggesting that an immunological mechanism is involved and that IgE may play an important role in the pathophysiology of the chemical-induced asthma.
In conclusion, the studies included in his doctoral thesis shed light on the pathophysiology of OA due to persulfate salts and propose a complex interaction of innate and a mixed type1-type2 adaptative immune response.
3
Gould, David James. "Leucocyte recruitment in a model of allergic airways disease." Thesis, University of Southampton, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.384947.
Testo completo
4
Varley, John Graeme. "Development of a model of allergic airways disease A." Thesis, University of Southampton, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385226.
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5
Zhang, Youming. "A genome-wide search for asthma-associated quantitative traits loci in a mouse model of allergic asthma." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312554.
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6
Huggins, Mary L. "A parasite model for lung eosinophilia." Thesis, University of Nottingham, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240928.
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7
Finlay, Alison. "Kinetics of pulmonary eosinophilia in a mouse model." Thesis, University of York, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245971.
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8
Stoten, Adam. "A model for non-atopic eosinophilic inflammation in the athymic rat." Thesis, University of Nottingham, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368238.
Testo completo
9
Seminario, Maria Cristina. "Development of a novel guinea pig model of allergic airways disease." Thesis, University of Southampton, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.239410.
Testo completo
10
Lee-Fowler, Tekla. "Determination of allergen sensitization and comparison of subcutaneous and mucosal (intranasal) allergen-specific immunotherapy in an experimental model of feline asthma." Diss., Columbia, Mo. : University of Missouri-Columbia, 2009. http://hdl.handle.net/10355/6723.
Testo completoAbstract (sommario):
Thesis (M.S.)--University of Missouri-Columbia, 2009.<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. "May 2009" Includes bibliographical references.
11
Schulz, Nikola. "microRNA profiling and target identification in a mouse model for allergic asthma." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-143012.
Testo completo
12
John, Elinor. "Lung function responses and mucus secretion in a model of chronic asthma." Thesis, Cardiff University, 2009. http://orca.cf.ac.uk/54093/.
Testo completoAbstract (sommario):
In summary, these observations demonstrate that lung function appears to be impaired by mucus secretion in an experimental animal model of chronic allergic asthma. The guinea pig model of chronic asthma may be utilised to investigate the development of a mucus hypersecretory phenotype in asthma or identify potential targets for the development of novel therapies aimed at reducing goblet cell mucus production or secretion.
13
Kintner, Eileen Kae 1957. "Testing of the school-aged child and adolescent acceptance of asthma model." Diss., The University of Arizona, 1996. http://hdl.handle.net/10150/282275.
Testo completoAbstract (sommario):
School-aged children and adolescents experiencing a chronic illness have verbalized and demonstrated difficulty in accepting their illness and the need for continued treatment. Few researchers have explored the school-aged child/adolescent process of acceptance. To assist school-aged children/adolescents toward acceptance, nurses must have a clear understanding of the process. This study is part of an ongoing program of research designed to increase nurses' understanding of the process of coming to accept asthma. The purpose of this study was to explore relationships among variables in the School-aged Child and Adolescent Acceptance of Chronic Illness Model. A Life-Span Developmental perspective guided the study. Multiple regression was used to test the theory. Concepts contained in the model were defined and operationalized, instruments were developed and/or identified, and relational statements were posed. The research question asked: What is the best linear path fit of the School-Aged Child and Adolescent Acceptance of Chronic Illness Model. The sample consisted of ninety-four school-aged children and adolescent diagnosed with asthma, between the ages of nine and fifteen years, and who were able to read and understand English. Subjects were recruited using the networking method. Path analysis determined the accuracy of the linear path model. Possible threats to validity of the model were examined. Results revealed school-aged child and adolescent acceptance of asthma was directly dependent upon one's perceived social support from his/her school teacher and classmates; and indirectly influenced by one's perceived social support from his/her parent, an objective measure of severity of illness rating, one's level of unrestricted participation in life activities, and one's perceived athletic competence. Results possess clinical and research implications for identifying, developing, and testing interventions to facilitate school-aged child and adolescent acceptance of asthma.
14
El-Hashim, Ahmed Zakaria. "Characterisation of acute and chronic airway hyperresponsiveness in an allergic rabbit model." Thesis, King's College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286197.
Testo completo
15
Schooley, Elizabeth K. "The effects of an antiseritonergic drug and antihistamine in an experimental model of feline asthma." Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/5033.
Testo completoAbstract (sommario):
Thesis (M.S.)--University of Missouri-Columbia, 2007.<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. Vita. "May 2007" Includes bibliographical references.
16
Lundquist, Gabriel, and Samuel Holmström. "Digital Treatment of Asthma Patients in Swedish Primary Care : A Business Model Study." Thesis, KTH, Skolan för industriell teknik och management (ITM), 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-279628.
Testo completoAbstract (sommario):
The cost of healthcare has been steadily increasing over the last decades and is becoming an increasing liability on the public finances. Much of these resources are directed to the primary care, and more specifically to the treatment of chronic diseases within the primary care. Digital healthcare, which has been highlighted as a potential way of increasing the efficiency within the primary care, has so far been unable to provide continuous care to patients with chronic diseases. New digital business models are needed to properly treat these patient groups. This study has evaluated the feasibility of a new digital business model for the treatment of the chronic disease of Asthma. The feasibility of business models was evaluated qualitatively from a patient, payer and provider perspective. Parameters for evaluating feasibility from the three perspectives were determined through policy reports as well as expert and practitioner interviews. Patient journeys, with their corresponding business models, were developed iteratively together in a series of interviews with practitioners from diverse disciplinary backgrounds. The evaluation of the business model’s feasibility for treating patients with asthma was done on a basis of clinical studies, clinician interviews, five patient interviews as well as financial calculations on provided care from the perspective of the provider and the payer. The study found that business models based on fee-per-action reimbursement, which are dominating in digital healthcare currently, are feasible for treating patients with mild asthma, but not for patients with severe asthma. For patients with severe asthma, business models based on capitation reimbursement are feasible, while the care can be provided 100% digitally by the inclusion of a bluetooth spirometer. A capitation based business model would provide better care for patients with severe asthma, to a lower cost to the payer (the healthcare region) and would be financially viable for the provider of healthcare. Our findings indicate that while asthmacare can be treated digitally with good patient outcomes as well as cost-efficiency, providers need to establish a physical presence in order to adopt a financially viable business model.<br>Sjukvårdens kostnader har stadigt ökat de senaste decennierna och har blivit en allt större belastning på de offentliga utgifterna. Mycket av dessa kostnader kommer från primärvården, och framförallt till insatser mot kroniska sjukdomar. Digital sjukvård, som ofta lyfts som ett möjligt verktyg för att minska vårdens kostnader, har hittills inte använts för att ge kontinuerlig vård till kroniker på bred skala. Nya digital affärsmodeller behövs för att behandla dessa patientgrupper. Denna studie har undersökt genomförbarheten av att behandla den kroniska diagnosen astma med digitala affärsmodeller. Genomförbarheten av de olika affärsmodeller utvärderades kvalitativt utifrån tre intressenters perspektiv: patienten, beställaren och vårdgivaren. Relevanta utvärderingsparametrar fastställdes genom myndighetsrapporter samt intervjuer med experter och praktiker. Patientresor, med tillhörande affärsmodell, utvecklades iterativt i intervjuer med praktiker från olika fält. Genomförbarheten av affärsmodellerna utvärderas slutligen med hjälp av resultat från kliniska studier, intervjuer med kliniker, intervjuer med patienter samt finansiella beräkningar på levererad vård utifrån beställaren och vårdgivarens perspektiv. Vi fann att digital affärsmodeller som får sin ersättning via utomlänspatientavgift är genomförbara för att leverera vård till patienter med mild astma, men inte till patienter med svår astma. För patienter med svår astma är digital affärsmodeller som bygger på kapiteringsersättning genomförbara. Kapiteringsersättning bygger på att vårdgivaren har fysisk närvaro, men vi fann att vården kan hanteras 100% digitalt till goda resultat för patienten, beställaren och vårdgivaren.
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Clark, Brenda Rose. "Development of an Air Pollution Asthma Risk-Screening Model for Ohio Elementary Schools." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1345233071.
Testo completo
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Allakhverdieva, Zoulfia. "Modulation of airway responses to antigen in a rat model of allergic asthma." [Montréal] : Université de Montréal, 2002. http://wwwlib.umi.com/cr/umontreal/fullcit?pNQ73468.
Testo completoAbstract (sommario):
Thèse (Ph. D.)--Université de Montréal, 2002.<br>"NQ-73468." "Thèse présentée à la faculté des études supérieures en vue de l'obtention du grade de philosophiae doctor (Ph. D.) en sciences biomédicales." Version électronique également disponible sur Internet.
19
Finney, Paul Anthony. "Development and characterisation of an in vivo model of β₂-adrenoceptor desensitisation in the rat". Thesis, Imperial College London, 1999. http://hdl.handle.net/10044/1/7671.
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20
Hutson, Penelope Ann. "Investigations into the mechanisms of late phase responses in guinea pig airways." Thesis, University of Southampton, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.328461.
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21
Lynch, Brittany. "Investigating the therapeutic potential of polyclonal antibodies in a murine model of allergic asthma." Thesis, Lynch, Brittany (2012) Investigating the therapeutic potential of polyclonal antibodies in a murine model of allergic asthma. Honours thesis, Murdoch University, 2012. https://researchrepository.murdoch.edu.au/id/eprint/41661/.
Testo completoAbstract (sommario):
Using the OVA mouse model of allergic airway disease, a histological grading system was established to evaluate four cardinal features of allergic asthma: Perivascular Inflammatory Cuffing, Peribronchial Inflammatory Cuffing, Goblet Cell Hyperplasia, and Tissue Eosinophilia. Using histochemical methods, this grading system was applied to identify a shallow dose response between allergen dose and resultant histopathology. This trend reached maximal effect with low doses of allergen and was observed in both perivascular and peribronchial cuffing thickness. A degree of goblet cell hyperplasia was observed in response to a low dose of allergen administration, but the dose response tended to plateau over the mid-range doses of allergen. Tissue eosinophilia was increased response to higher doses of allergen. In an investigation of the immune exclusionary capacity of Ruminant Polyclonal Antibodies (RPA), the histological grading system was applied to evaluate whether histopathological changes could be influenced or decreased by polyclonal antibodies. A non-specific action of allergen-specific Immunoglobulin G was identified. A pro-inflammatory tendency of an antibody:allergen complex was identified, and lung inflammation occurred as a result. These studies indicate the possibility that antibodies are able to act in an exclusionary manner at mucosal surfaces.
22
Ghosh, Sumit. "Immunomodulatory Role of B Lymphocytes and Hyaluronic Acid in a Murine Model of Allergic Asthma." Diss., North Dakota State University, 2012. https://hdl.handle.net/10365/26663.
Testo completoAbstract (sommario):
In the world today, asthma affects more than 235 million people. The widespread prescription of inhaled corticosteroids?the current gold standard of asthma control medication?allows many asthmatics to live symptom-free and has significantly reduced the number of deaths due to asthma. However, when the disease is poorly controlled, for example due to ubiquitous exposure to airborne fungal conidia, this chronic inflammatory disease often results in lung dysfunction caused by airway architectural changes. The role of B lymphocytes in allergic asthma has been relegated to the production of IgE with relatively little being known about the trafficking of these cells in the tissues or their role(s) in the affected tissue. As a first step in ascertaining their function, the initial aim of this project was to characterize the recruitment and localization of B cells in the murine lung in response to Aspergillus fumigatus inhalation. We found that CD19+CD23+ B2 lymphocytes were recruited to the lungs after fungal inhalation and that IgA-, IgE-, IgG-producing cells localized around the large airways. The second aim of the project was to begin defining the impact that these B lymphocytes have on the allergic lung. By using mice that were deficient of conventional B cells, we were able to demonstrate that the allergic phenotype was retained, although the impact of tissue B1 B cells cannot yet be ruled out. We then investigated the ability of hyaluronic acid (HA), a major component of the extracellular matrix (ECM) generated at sites of chronic inflammation, to recruit and modulate B lymphocyte functions in allergic fungal disease. We found that B lymphocytes undergo chemotaxis in response to LMM HA, while HMM HA had little to no effect on B cell chemotaxis. Furthermore, HA-mediated B lymphocyte chemotaxis was significantly inhibited by blocking the CD44 HA receptor. We also demonstrated that LMM HA fragments elicit the production of the pro-fibrotic cytokines IL-10 and TGF-?1 by B lymphocytes. These observations suggest a previously unrecognized role for B lymphocytes and HA in the context of allergy and represent novel pathways by which B lymphocytes may contribute to airway inflammation and airway remodeling.
23
Oberholzer, Nanette. "Evaluation of the anti-inflammatory properties of a complex homeopathic product Modul8® using the BALB/c murine asthmatic animal model /." Access to E-Thesis, 2009. http://upetd.up.ac.za/thesis/available/etd-04292010-092056/.
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24
Evaldsson, Chamilly. "Uridine, 4-thiouridine and isomaltitol in an asthma-like model : Anti-inflammatory and modulating effects." Doctoral thesis, Linköpings universitet, Klinisk kemi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-19122.
Testo completoAbstract (sommario):
In chronic inflammatory diseases like asthma or rheumatoid arthritis, erroneous and exaggerated accumulation of leukocytes in a tissue inadvertently causes the body harm. Several efficient anti-inflammatory drugs exist, for example corticosteroids and cyclo-oxygenase inhibitors. However, these drugs have potent and diverse effects and often act by inhibiting events subsequent to initiation of the inflammatory response, leading to more or less severe side-effects, especially when used in high doses for long periods of time. For this reason, strategies aimed at early inhibition of recruitment and activation of leukocytes have been suggested as safer and more specific approaches to reduce inflammation. Leukocyte adhesion to activated endothelium is a prerequisite to the following activation and extravasation, and takes place in the initial phase of inflammation. By using a model that allows leukocytes to adhere to tumour necrosis factor (TNF)-activated endothelial cells, thus mimicking aspects of an inflammatory reaction, we found that uridine, 4-thiouridine and isomaltitol could all reduce adhesion. This suggested that they may have anti-inflammatory potential. We therefore tried the three substances in a Sephadex-induced lung inflammation model and found that uridine and 4-thiouridine have several anti-inflammatory effects, such as being able to reduce leukocyte accumulation, decrease TNF protein levels and partly inhibit the oedema induced by Sephadex. Isomaltitol turned out to have immunomodulating, rather than anti-inflammatory, effects, which could be of interest in diseases where inadequate inflammatory responses are a problem.
25
Wong, Pei Se. "Development of a pharmaceutical care model for the long-term management of asthma in Malaysia." Thesis, University of Strathclyde, 2012. http://oleg.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=16855.
Testo completoAbstract (sommario):
Asthma is one of the most common chronic diseases affecting adults and children in the world. To date, it is estimated to affect over 300 million of the world population and presents a significant healthcare burden in all countries. In the United State (US) and Europe, asthma control is reported to be achievable by only 5% of asthmatics. Asthma is also one of the top 5 conditions, which impact on healthcare expenditures in the US. Asthma affects 4.6% of the population in Malaysia and has major effects on morbidity, mortality and healthcare costs. The development of a pharmaceutical care model for the long-term management of asthma patients in Malaysia has the goal of increasing patients’ and professionals’ levels of understanding of the pharmacological management of the disease, by developing a framework for the provision of pharmaceutical care. Within that framework, pharmacy services are aimed at promoting the management of prescribed medicines and securing better disease control through decision support and education provided to other health professionals and patients. The overall aim of the current research is to develop a pharmaceutical care model for the long-term management of asthma in Malaysia. This thesis presents the series of research studies undertaken to achieve the aim of study. Chapter 1 of the thesis reviews the intention of the research plan and provides insights into the disease of asthma. The status of the healthcare system in Malaysia and the concept of pharmaceutical care are also discussed. Chapter 2 and Chapter 3 of the thesis discuss the assessment of pharmaceutical needs by means of quality assessment using clinical audit and a direct patient-facing clinical exploratory method. A design and validation processes generated a tool, an Asthma Medication Assessment Tool (MATAST) that can be used not only for quality assessment purpose, but comparison at the international level. The field-testing process of the MAT provides preliminary insights into gaps in asthma clinical management and, potentially, the need for decision support. The direct patient-facing clinical exploratory study uses two methods; semi-structured interviews with individual patients and focus groups of patients to improve understanding of patients’ needs. The outcomes of these studies are a list of gaps of care from clinical audit and patients’ views or perceptions from patients’ interviews which are critically appraised in Chapter 4. Chapter 5 of the thesis discusses a consensus process used to establish a pharmaceutical care model and roles of pharmacists in that model of care. The objective of the consensus process is to establish the activities for in a pharmaceutical care model for asthma management in Malaysia. This study also includes a consensus process of the agreed activities by pharmacists within the pharmaceutical care model. Chapter 6 presents a study to evaluate the self-management ability of patients by means of an educational intervention using an action plan. Asthma self-management is a globally relevant component of care, which is not commonly practised in Malaysia and has never been studied in this country. This study revealed ways of improving the action plan and the patients use of it; the findings provide a framework for asthma self-management interventions in Malaysia. Chapter 7 critically appraises the implications of the findings in the thesis for practice and education as well as future research in the provision of pharmaceutical care in the asthma population.
26
Jessop, Donna Catherine. "The Self-Regulatory Model and its application to asthma and adherence to inhaled preventative medication." Thesis, University of Kent, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297343.
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Hafezi, Nazila. "An integrated software package for model-based neuro-fuzzy classification of small airway dysfunction." To access this resource online via ProQuest Dissertations and Theses @ UTEP, 2009. http://0-proquest.umi.com.lib.utep.edu/login?COPT=REJTPTU0YmImSU5UPTAmVkVSPTI=&clientId=2515.
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Spong, Amanda J. "Are children's thoughts and feelings about illness related to medication use and symptom control? : an examination of the self regulatory model." Thesis, University of East Anglia, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327135.
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29
Lulham, George W. "The effect of cytokine administration on treatment and prevention of asthma in a sensitized mouse model." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0008/NQ52173.pdf.
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30
Lam, Diane Phuong Nghinh. "Characterization of the immunomodulatory activities of sterile house dust extracts in a murine model of asthma." Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p1447798.
Testo completoAbstract (sommario):
Thesis (M.S.)--University of California, San Diego, 2008.<br>Title from first page of PDF file (viewed Feb. 5, 2008). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 60-66).
31
Strangman, Wendy K. "Anti-inflammatory capabilities of compounds from marine bacteria in a mouse model of allergic inflammation and asthma." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2007. http://wwwlib.umi.com/cr/ucsd/fullcit?p3284210.
Testo completoAbstract (sommario):
Thesis (Ph. D.)--University of California, San Diego, 2007.<br>Title from first page of PDF file (viewed March 14, 2007). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
32
Schulz, Nicola [Verfasser], and Elisabeth [Akademischer Betreuer] Weiß. "microRNA profiling and target identification in a mouse model for allergic asthma / Nikola Schulz. Betreuer: Elisabeth Weiß." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2012. http://d-nb.info/1022523953/34.
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Alrifai, Mohammed [Verfasser], and Holger [Akademischer Betreuer] Garn. "Resolution of airway remodelling in a mouse model of chronic allergic asthma / Mohammed Alrifai ; Betreuer: Holger Garn." Marburg : Philipps-Universität Marburg, 2019. http://d-nb.info/1183909020/34.
Testo completo
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Musaad, Salma MA. "Anthropometric Measures of Obesity and the Association with Asthma and Other Allergic Disorders: Cincinnati Children’s Allergy and Immunology Clinic Cohort." University of Cincinnati / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1192570691.
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Steffan, Breanne. "Interactions of Aspergillus fumigatus and Pseudomonas aeruginosa Contribute to Respiratory Disease Severity and Death." North Dakota State University, 2019. https://hdl.handle.net/10365/31346.
Testo completoAbstract (sommario):
The lung was recently identified to consist of a complex microenvironment made up of microorganisms that interact with one another and the host cells via direct and indirect interactions. As a result, understanding the dynamic of the microbiome in chronic respiratory diseases has become the focus of pulmonary researches. In cystic fibrosis (CF), chronic infections are a comorbidity associated with the genetic disorder. Recently, it was noted that the interactions of the fungus, Aspergillus fumigatus, and the bacterium, Pseudomonas aeruginosa together contribute to more severe disease outcomes in CF patients. In vitro co-cultures show that P. aeruginosa and A. fumigatus can affect one another’s growth and pathogenicity, but very few studies have attempted to model interactions of these microorganisms in vivo. Based on clinical and basic research, we developed a co-exposure model in which we could compare non-allergic and allergic animals co-exposed to Pseudomonas aeruginosa and Aspergillus fumigatus. While both groups had significant neutrophilia and production of acute phase response cytokines and chemokines, the allergic co-exposed group had a greater mortality with 34.8% of the animals expiring by 24h in comparison to 12.5% for the non-allergic co-exposed animals and 100% survival in the controls. A contributing factor to the more severe disease outcomes in the allergic co-exposed group is the increase in eosinophilic inflammation and IL-17A production, which only occurs when both microorganisms are viable. In addition, it was found that viable P. aeruginosa but not A. fumigatus causes interstitial inflammation, significant neutrophilia, and even death during co-exposures. The decline in health of animals co-exposed to the fungus and bacteria could be attributed not only to the host’s inflammatory response, but also to the spatial and temporal co-localization in the lung. To address this, we performed in vitro studies finding an aggregation of the microorganisms that could also be identified in vivo. This current research emphasizes the need for in vivo studies on polymicrobial interactions.<br>ND Agricultural Experiment Station; National Institute of Allergy and Infectious Diseases of the National Institutes of Health under Award Number R155AI137886
36
Molter, Anna. "Air pollution exposure and respiratory health in childhood." Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/air-pollution-exposure-and-respiratory-health-in-childhood(86388151-13d1-499d-be59-89d6d87e036f).html.
Testo completoAbstract (sommario):
Asthma is the most common chronic disease in children and the effects of air pollution exposure on asthma and respiratory health in children have been a growing concern over recent decades. Although a number of epidemiological studies have been carried out in this field, these have produced conflicting results. The aim of this study was to assess the effects of long term exposure to nitrogen dioxide (NO2) and particulate matter (PM10) on asthma prevalence and lung function in children. To achieve this, a novel exposure model was developed and evaluated, which allowed retrospective exposure assessment of children participating in a population based birth cohort study – the Manchester Asthma and Allergy Study (MAAS). MAAS is a prospective birth cohort study comprising 1185 children specifically designed to study asthma and allergies. Clinical follow up took place at ages 3, 5, 8 and 11 years. At each follow up parents completed questionnaires on asthma diagnosis and symptoms and children underwent skin prick tests for common allergens. Children’s specific airways resistance (sRaw, at ages 3, 5, 8, 11) and forced expiratory volume in one second (FEV1, at ages 5, 8, 11) were measured. At ages 5 and 11 years FEV1 was measured at baseline and after bronchodilator treatment. The exposure model developed during this study incorporated outdoor and indoor air pollution, spatio-temporal variation in air pollution and time-activity patterns of children. The model was based on the concept of microenvironmental exposure. It modelled personal exposure based on PM10 and NO2 concentrations in children’s home, school and journey microenvironments (MEs) and the length of time they spend in these MEs. Land use regression (LUR) models were used to model PM10 and NO2 concentrations in outdoor MEs. These LUR models were specifically developed for the Greater Manchester area. A novel method was used to develop the LUR models, which used the output from an air dispersion model as dependent variables in the regression analysis. Furthermore, a novel approach was used to obtain annual concentration of PM10 and NO2 from 1996 to 2010, which involved the recalibration of the LUR models for each year. A mass balance model and indoor to outdoor ratios were used to model concentrations in indoor MEs. The performance of the exposure model was evaluated through a personal monitoring study in schoolchildren attending a local secondary school. Children wore personal NO2 monitors for two consecutive days in four seasons. Parental questionnaires and time-activity diaries were used to obtain information for the exposure model and to model NO2 exposure for the same time period. The results showed good agreement between monitored and modelled NO2 concentrations (Normalised mean bias factor=-0.04). Multiple linear regression and generalised estimating equations (GEE) were used to assess the cross-sectional and longitudinal effect of modelled exposure on sRaw and FEV1 (as % predicted). Multiple logistic regression and GEE were used to assess the effect of modelled exposure on the prevalence of asthma and current wheeze.The longitudinal analyses showed significant associations between PM10 and NO2 exposure and % predicted FEV1 (PM10: B=-1.37, p=0.019; NO2: B=-0.83, p=0.003), but no association with sRaw (PM10: B=0.009, p=0.37; NO2: B=-0.007, p=0.16). The cross-sectional analyses showed no association between pollutant exposure during the summer or winter prior to age 11 and any of the lung function measures (p>0.05). Long term PM10 or NO2 exposure were not associated with asthma or current wheeze (p>0.05).This study developed and evaluated a novel air pollution exposure model for epidemiological research. The results of this study suggest a negative impact of long term exposure to NO2 and PM10 on growth in FEV1 during primary school age. However, no evidence of an association between long term exposure to NO2 and PM10 and childhood asthma was found.
37
Tamulis, Tomas. "Association between area socioeconomic status and hospital admissions for childhood and adult asthma." [Tampa, Fla.] : University of South Florida, 2005. http://purl.fcla.edu/fcla/etd/SFE0001134.
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Ceresa, Claudia Carla. "Use of a three dimensional cell culture model to study airway smooth muscle - mast cell interactions in asthma." Thesis, University of Nottingham, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.602487.
Testo completoAbstract (sommario):
Asthma is a disease that still causes a significant amount of morbidity and mortality in the UK. Airway smooth muscle hypertrophy and hyperplasia, with a corresponding infiltration by mast cells, are key features of the inflammatory process that results in airway remodelling and fixed airflow obstruction. A 3 dimensional collagen I model was developed to examine differences in airway smooth muscle cell morphology, phenotype and MMP 2 expression, when cultured in a 30 environment in comparison to a 20 monolayer. Using :: this technique, airway smooth muscle cells and HMC-1s, a mast cell line, ,; were co-cultured to assess the effects of cell to cell interaction on airway I smooth muscle proliferation rates and MMP2 production. A novel method for assessing HMC-1 migration towards airway smooth cells was also established. To further study mast cell migration in asthma, a new technique of patient recruitment and endobronchial biopsying of individuals had to be established. Airway smooth muscle cells when cultured in 30 were observed to adopt a spindle like morphology. They also appeared to express lower levels of a smooth muscle actin and vimentin. In the model, basal rates of airway smooth muscle cell proliferation, when examined using Ki67, are reduced by over 50% compared to the 20 controls (p<0.05). Rates of airway smooth muscle cell proliferation were significantly increased in the model when they were co-cultured with the HMC-1s, and activated HMC-1s; the rate doubling in the latter from sole culture alone (p<0.05). 6 --. ---------- - Culturing airway smooth muscle cells in 3D also resulted in increased and sustained MMP2 production with a further increase when co-cultured with HMC-1s. This also resulted in increased expression of the activated form. Co-culturing of the cells resulted in increased rates of gel contraction, by 22%. This contraction could be reduced by using a broad spectrum MMP inhibitor, 1I0mastat. HMC-1 migration towards airway smooth muscle is partially MMP dependent. The rate of HMC-1 s migrating when treated with 1I0mastat was reduced by 45% (p<O.05). Initial studies of migration of HMC-1s to asthma derived airway smooth muscle cells showed up to 66% increase in migration compared to non-asthmatic controls, and that there is a trend towards increased proliferation in this group. Asthma airway smooth muscle cells also promoted gel contraction. 7
39
Rate, Angela. "Epithelial cell regulation of dentritic cell maturation in the airway mucosa : studies in an in vitro model system." University of Western Australia. School of Paediatrics and Child Health, 2009. http://theses.library.uwa.edu.au/adt-WU2009.0206.
Testo completoAbstract (sommario):
[Truncated abstract] Atopic asthma pathogenesis is driven by the combined effects of airway inflammation generated during responses to viral infections and aeroallergens, and both of these pathways are regulated by dendritic cells (DC) that differentiate locally from monocytic precursors. These DC normally exhibit a sentinel phenotype characterised by active antigen sampling but attenuated presentation capability, which limits the intensity of local expression of adaptive immunity. How this tight control of airway DC functions is normally maintained and why it breaks down in some atopics leading to immunopathological changes in airway tissues, is unknown. In the airway mucosa, DC are intimately associated with airway epithelial cells (AEC), which are a source of a range of both pro- and anti-inflammatory mediators. A few studies have previously examined the effects of AEC-derived surface-expressed and soluble mediators upon the function of pre-differentiated DC, although there is a dearth of information as to the extent of AEC-conditioning of DC during their generation from incoming monocytic precursors within the airways. Therefore, this study was designed to test the hypothesis that signals from adjacent AEC contribute to regulation of local differentiation of airway mucosal DC, especially in the context of allergic airway disease. A direct co-culture model was developed containing the AEC line 16HBE 14o- as a surrogate for primary AEC, and purified peripheral blood monocytes derived from atopic patients in a GM-CSF/IL-4-enriched cytokine milieu. Cells were cultured for 5 days, at which time the phenotype and functional attributes of the monocyte-derived DC (MDDC) generated in the presence of AEC (AEC-MDDC) were compared to the control MDDC population generated without AEC contact (Ctrl- MDDC). ... In parallel, an attenuation of mRNA boosting for 7 out of 12 selected Th2-asscociated genes as well as IL-13 protein, was observed in AEC-MDDC supplemented cultures compared to ctrl-MDDC supplemented cultures. The data collected in the initial characterisation of the AEC-MDDC in Chapter 3 and further analysis of their gene expression profiles by microarray suggest a number of DC-associated factors could be involved in directing a potential bias against Th2 immunity within the T-cell recall response. These include increased expression of IL- 12 subunit mRNA and the enhanced levels of surface MHC Class II, CD80, ICAM-1 and SLAM. Further to Th1/Th2 modulation, a number of T-regulatory (Treg) genes were differentially expressed in the AEC-MDDC-re-activated CD4+ T-cells, and members of the chemokine and metallothionein families were elevated in the same population. Collectively the results of this study suggest that in the context of the atopic airway microenvironment where there is an abundance of Th2-related mediators, healthy AEC arm locally maturing DC with an arsenal of anti-microbial defences that can be rapidly employed in response to encounter with inhaled pathogens, in particular viruses. In this way, the DC are maintained in an ideal functional phenotype to efficiently mobilise both innate and Th1-polarised adaptive immune defences against infection, whilst achieving tight control of potentially-damaging Th2 immunity to aeroallergens, thus contributing to the maintenance of immunological homeostasis within the respiratory tract.
40
Buckley, Tyra T. "Delivery of Asthma Management Services by a Federally Qualified Health Center in an Urban Setting." Digital Archive @ GSU, 2010. http://digitalarchive.gsu.edu/iph_theses/145.
Testo completoAbstract (sommario):
As a chronic disease, asthma presents a significant public health challenge nationally and in Georgia. In 2007, over 22 million people, including over 9 million children, had asthma in the United States. In Georgia, 230,000, or 10% of children have asthma, which is more prevalent among children less than 18 years of age than among adults. While asthma affects people of all ages and socioeconomic status, low income and minority populations have the highest asthma morbidity. This has proven to be the case with residents of Neighborhood Planning Unit V (NPU-V), a low-income minority community located in southeast Atlanta. Children comprise 35% of NPU-V's population, and over half of them live below the poverty line. Among other concerns, children with asthma have higher rates of hospitalization and absenteeism from school than their peers. The hospitalization rates for children with asthma in South Atlanta aged 0-17 years of age is almost five times the rate of North Fulton County. The Georgia State University Institute of Public Health received grant funding for the planning and implementation of the Accountable Communities: Healthy Together-Asthma (ACHT-A) program to help address the problems associated with asthma in NPU-V and among patients of Southside Medical Center (SMC). The capstone project involved development of an evaluation plan for future determinations about the program’s effectiveness in achieving desired outcomes. The evaluation process included development of a logic model and putting systems in place to track and measure specific indicators. The project culminated in a preliminary assessment of selected program activities to establish baseline information for the program, its participants, and SMC staff.
41
LeBlanc, Lawrence Joseph. "CFD evaluation of cluster specific image based asthma lung features on particle transport and hygroscopic particle growth model validation." Thesis, University of Iowa, 2017. https://ir.uiowa.edu/etd/5546.
Testo completoAbstract (sommario):
Aerosolized drug delivery to the human lungs for asthma treatment has long been studied and yet the relationship between the delivery efficacy and the inter-subject variability due to gender, age, and disease severity remains unclear. A recent imaging-based cluster analysis on a population of asthmatic patients identifies four clusters with distinct structural and functional characteristics. The use of cluster membership to explore inter-subject variability by investigating numerically the air flow and particle transport in representative subjects of the asthmatic clusters on inhalation drug delivery in asthma sub-populations is proposed. Large-eddy simulations using computed tomography (CT)-based airway models were performed with a slow and deep breathing profile corresponding to application of a metered dose inhaler. Physiologically consistent subject specific boundary conditions in peripheral airways were produced using an image registration technique and a resistance network compliance model. Particle simulations and final deposition statistics were calculated for particle sizes ranging from 1–8 μm. The results suggested an emphasis on the importance of airway constriction for regional particle deposition and prominent effects of local features in lobar, segmental, and sub-segmental airways on overall deposition patterns. Asthmatic clusters characterized by airway constriction had an increase in deposition efficiency in lobar, segmental, and sub-segmental airways. Local constrictions produced jet flows that impinged on distal bifurcations and resulted in large inertial depositions. Decreased right main bronchus (RMB) branching angle decreased the fraction of particles ventilated to the right upper lobe (RUL). Cluster-based computational fluid dynamics results demonstrate particle deposition characteristics associated with imaging based variables that could be useful for future drug delivery improvements.
One method for circumventing low deposition in small airways due to constriction in tracheobronchial airways is through hygroscopic growth of aerosols for inhalation. Hygroscopic materials have an affinity for water and can enlarge in size significantly as they traverse through respiratory tract. Hygroscopic growth has shown promise as a viable drug delivery method for decreasing deposition in the upper tracheobronchial region and increasing drug penetration and retention in small airways. Current models for hygroscopic growth models show promise in predicting steady state final diameter aerosol droplet sizes, but much uncertainty in predicting transient effects exists. This paper discusses in detail one such growth model and modifies it to include realistic spatial temperature and humidity variations associated with the lung. The growth model is simplified through grouping of terms and is then solved using MATLAB ODE 45 solver. The model is compared to experimentally acquired in vitro data for validation. The results do not show good agreement with the model, and suggests that additional factors exist that inhibit aerosol droplet growth from commencing immediately upon entering the respiratory tract like is assumed true in literature. This paper briefly hypothesizes for reasons for model and data disagreement and limitations of current growth models.
42
Shaw, Ina. "Development of a management model for the treatment of asthma." Thesis, 2010. http://hdl.handle.net/10210/3220.
Testo completoAbstract (sommario):
D.Phil.<br>Asthma exemplifies a major medical concern and is a considerable cause of morbidity and mortality globally and in South Africa. Biokineticists have in the past primarily prescribed aerobic modes of exercise to asthmatics regardless of other modes of exercise that could be used in the management of asthma, each with their own unique benefits. The aim of this investigation was to develop a management model from a biokinetic perspective for the management of asthma in moderate, persistent asthmatics. The present study utilised a quantitative, comparative, research trial making use of a pre-test, eight-week intervention period and a post-test. Eighty-eight sedentary moderate, persistent asthmatics were matched by age and gender and randomly assigned to either a non-exercising control group (NE) (n = 22), an aerobic exercise group (AE) (n = 22), a diaphragmatic inspiratory resistive breathing group (DR) (n = 22) or an aerobic exercise combined with diaphragmatic resistive breathing group (CE) (n = 22). Dependent t-Tests and rank-ordered analyses revealed that five of the 13 pulmonary function parameters assessed were found to be significantly altered following the AE and CE training, with the CE training having a larger impact than AE training. The DR training resulted in improvements in four of the 13 pulmonary function parameters. The CE and AE training were also found to be equally effective at altering physical work capacity, while the DR training proved ineffective at altering physical work capacity. The CE training proved to be the most effective at improving the abdominal and chest wall excursion parameters. The DR training was found to be the least effective mode of exercise training to impact favourably on abdominal and chest wall excursion parameters. The DR and CE training had a similar significant and favourable change in respiratory muscle flexibility followed by the AE training only impacting on nine of the 11 respiratory muscle flexibility parameters. Regarding the respiratory muscle strength, despite AE and CE training altering 18 of the 20 parameters, CE training was found to be more effective. DR training only altered 16 of the 20 respiratory muscle strength parameters. The DR training was the only modality to alter a postural parameter, albeit unfavourably. Even though the DR and AE training significantly altered four of the six anthropometric parameters, the AE training proved to be superior, while CE training proved least effective as it altered v only three of the measured anthropometric parameters. The overall success of the CE training exemplified the fact that an optimal training regime for the management of asthma may require both an aerobic exercise and diaphragmatic inspiratory resistive breathing component. Exercise training, and specifically CE training is a cost-effective, home-based asthma management programme that may reduce the public health burden of this disease and provide the patient with alternative treatment options. CE training should form the cornerstone in the management of asthma to minimise and prevent asthma exacerbations and thus improve health-related quality of life and may even prove to be life-saving.
43
Chen, Sue Hsien, and 陳淑賢. "Effects of an Integrative Asthma Care Model on Primary Caregivers’ Asthma Management and Children’s Health Control." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/60147750576241290061.
Testo completoAbstract (sommario):
博士<br>長庚大學<br>臨床醫學研究所<br>101<br>Parents or primary caregivers play an important role in care with asthmatic children. Caregivers without adequate knowledge in asthma care may affect the disease control and delay treatment. The purpose of this study was to evaluate the effect of an integrative asthma care model , which in composition with empowerment concept on primary caregivers’ asthma management and children’s health control. The study was conducted from December 2010 to August 2012 in the outpatient department of a medical center in northern Taiwan. The study subjects included asthmatic children (5-14 years of age) with no other systemic diseases, and the primary caregiver for these afflicted children. We randomized all subjects into three groups: Experiment Group A, Experiment Group B and Control Group. During the 3-month care period, subjects in Group A received regular care, four telephone interviews and individual instruction; subjects in Group B received clinical regular care, four telephone interviews and group instruction; and subjects in Control Group received ordinary instructions alone. One hundred and thirty subjects completed the pretest, including 44 in Group A, 24 in Group B and 62 in Control Group. At the end of the study, 68 subjects completed follow-up evaluation at the third month, the sixth month, the ninth month and the twelfth month, including 22 in Group A, 21 in Group B and 25 in Control Group.
We found that either individual or group instruction was helpful in care of asthmatic children and primary caregivers' asthma management improved markedly at the twelfth month. Both Groups A and B improved knowledge of asthma care significantly more than the Control Group (β=0.30, SE=0.11, p＜0.05；β=0.13, SE=0.12, p＞0.05) and the average score of Group A was higher Group B and the Control Group. In the attitude of asthma care, the highest average score was seen in Group A, and there was more improvement in Groups A and B than the Control Group (β=0.36, SE=0.11, p＜0.05；β=0.01, SE=0.11, p＞0.05). Concerning behaviors of asthma care, the lowest average score was found in the Control Group, and the change was much higher in Groups A and B than the Control Group (β=0.67, SE=0.39, p＞0.05；β=0.29, SE=0.36, p＞0.05). In emotions of asthma care, three groups in the post intervention had improved, and there was much more improvement in Group A and B (β= -0.43, SE=0.36, p＞0.05；β=-0.62, p＞0.05). Furthermore, three groups with intervention had significantly increased the Physician-Patient Communication as compared to those with no intervention, and the improvement was more significant in Experimental Groups A and B than the Control Group (β=0. 42, SE=0.16, p＜0.05；β=0.23, SE=0.16, p＞0.05).
To evaluate the Children’s Health Control, we assessed changes in pulmonary function and found that Groups A and B had changed higher than the Control Group in FVC (β=0.75, SE=0.32, p=0.02；β=1.17, SE=0.39, p＜0.01) and FEV1 (β=0.55, SE=0.29, p＞0.05；β=0.89, SE=0.35, p＜0.05). We used exhaled nitric oxide (eNO) to assess airway inflammatory conditions. Although there was no difference among these three groups (p> 0.05, Chi-square test), the number of airway inflammations of the control group increased. Additionally, methacholine challenge test was detected statistically significantly in the three groups (x2=6.83, p<0.05). During the study period, seven subjects (23.5%) went to the emergency room for asthma, Group A had a lower rate of emergency room use, and four subjects (13.2%) of the Control Group were hospitalized. There were significant differences between the three groups in terms of the number of hospital admissions(x2=7.31, p=0.03). In medication use for asthma, we found significant differences in the frequency of the use of oral corticosteroids or Montelukast among the three groups (p<0.05). However, we were unable to detect the difference in inhaled β-agonist use (p>0.05). Subjects in Groups A and B had more improvement in quality of life than the Control Group (β=1.27, SE=0.46, β=1.21, SE=0.47, p＜0.05). Particularly, the group instruction showed the best improvement in the quality of life.
The study quoted that the concept of empowerment in integrative asthma care model, through dialogue, listening and interactive process, guided reflection, and enhanced insight on children and disease control. The present study suggests that applying an integrative care program indeed improved primary caregivers’ management in asthma children and their health. Following this care model, we are able to strengthen children-centered care and provide continued integrity of care. We believe that an integrative asthma care model on primary caregivers’ asthma management and children’s health control is helpful.
44
Yu-Ling, Wu, and 吳玉琳. "The Immunoregulatory Effects of Propolis on Asthma Animal Model." Thesis, 2003. http://ndltd.ncl.edu.tw/handle/95423893194043323558.
Testo completoAbstract (sommario):
碩士<br>輔仁大學<br>食品營養學系<br>91<br>The frequency of allergic diseases such as asthma has increased rapidly during the past decade. Many studies indicated that cytokines secretion pattern trend to Th2 (type 2 helper T cells) response were noted on asthma disease. The aim of this study will focus on the effects of propolis in the animal model of asthma. BALB/c female mice were divided into four groups including control group, low (1.3 mg/day) or high (6.5 mg/day) dose propolis group, and non-treat group which referred as the unimmunized group. Mice were immunized and sensitized expose to ovalbumin (OVA) antigen, and administered with propolis by tube feeding or not. The serum OVA-specific antibody titer, cytokine, and chemokine prolifile in the supernatant of peritoneal exudation cells, splenocytes, and bronchoalveolar lavage fluid (BALF) were analized. The numbers of eosinophil in the BALF were established. The results showed that the propolis could suppress OVA-specific IgE and IgG1 level in sera, and airway hyperresponsiveness (AHR). There were no differences for the concentration of eotaxin or eosinophilia in BALF among four groups. The asthma animal model receiving propolis had shown decreased secretion of the proinflammation cytokines, such as IL-1β and IL-6. The propolis-administered mice (low and high dose groups) present strongen inhibition of IL-10 and upregulation of IFN-γ secretion of splenocytes stimulated with Con A (concanavalin A). In addition, the cytokine secretion patterns (such as IFN-γ, IL-1β, IL-4, IL-6, and IL-10) of OVA-sensitized splenocytes from propolis-administered groups were significantly lower than control group. This study may provide novel applicable therapy for those patients suffer from allergic asthma. The mechanism of immunoregulatory effect of propolis on Th2 cytokine worth further investigation.
45
Kapeleris, Audrey. "The Role of Hepoxilins in an Asthma-like Mouse Model." Thesis, 2010. http://hdl.handle.net/1807/24586.
Testo completoAbstract (sommario):
Asthma is a chronic respiratory illness where the airway occasionally constricts, becomes inflamed, and is lined with excessive amounts of mucus. There are many lipid mediators involved in this inflammatory response. Hepoxilins are biologically active hydroxyepoxy eicosatrienoic acid metabolites of arachidonic acid, formed through the 12-lipoxygenase pathway. Our goal in this study was to identify if hepoxilins had a direct effect on smooth muscle contractions, to identify the source of hepoxilins in asthmatic-like mouse model, and to determine if blocking this pathway reduced inflammation associated with ovalbumin sensitization. We found that hepoxilins had no direct effect on smooth muscle contraction. We identified the bronchiolar epithelium as a major source of hepoxilins in OVA-challenged mice. We demonstrated that baicalein inhibits total lung resistance in the OVA-treated mice, but also found that the drug in-vivo is not specific for 12-lipoxygenase.
46
Jui-ChangLiu and 劉瑞璋. "The effects of atorvastatin on foamy macrophage inchronic asthma mouse model." Thesis, 2019. http://ndltd.ncl.edu.tw/handle/s3ngxw.
Testo completo
47
Tatari, Nazanin. "The effect of semaphorin 3E on angiogenesis in murine model of allergic asthma." 2015. http://hdl.handle.net/1993/30967.
Testo completoAbstract (sommario):
Increased angiogenesis is an important characteristic of remodeling in asthmatic airways which stems from the imbalance between pro-angiogenic and anti-angiogenic factors. Surprisingly, the factors regulating this process in allergic asthma are poorly defined. The focus of this thesis is to investigate the effect of Semaphorin 3E (Sema3E) on angiogenesis events within the airways of murine model of allergic asthma.
The role of Sema3E in asthma angiogenesis was tested in wild type and Sema3e-/- mice exposed to House Dust Mite (HDM) and monitored for changes in blood vessels number in the lungs. In addition, the potential of Sema3E, in reversing features of allergen inflammation, was tested in mouse model. In both cases immunohistochemistry and immunofluorescence staining of lung tissues used to assess the changes in the level of angiogenesis. Moreover, the expression of pro- and anti-angiogenic factors in total lung homogenate was assessed by ELISA and Real-Time PCR.
The results showed that WT and Sema3e-/- mice both developed the HDM induced allergic asthma phenotype, but, the lung sections of HDM exposed Sema3e-/- mice had enhanced number of blood vessels compared to WT mice. The enhanced angiogenesis in Sema3-/- mice was coupled with increased level of angiogenesis driving factors VEGF and it receptor VEGFR-2. However, in WT mice the level of soluble VEGFR-1 secretion increased significantly which inhibited VEGF / VEGFR-2 binding.
Besides, Sema3E treatment reduced the level of angiogenesis and inhibited HDM-induced secretion of VEGF and the expression of its receptor VEGFR-2 while increased the level of soluble VEGFR-1. Analyzing the ratio of VEGF / soluble VEGFR-1 revealed that in the presence of Sema3E in both models, soluble VEGFR-1 is the dominant factor which has an inhibitory role on angiogenic effect of VEGF.
Taken together, this study provided the first evidence that Sema3E can modulate angiogenesis in allergic asthmatic airways.<br>February 2016
48
Herbert, Cristan Medical Sciences Faculty of Medicine UNSW. "Effects of glucocorticoid and phosphodiesterase-4 inhibitor therapy in a mouse model of chronic asthma." 2007. http://handle.unsw.edu.au/1959.4/40535.
Testo completoAbstract (sommario):
Asthma is a chronic inflammatory disease of the airways. Using a murine model which replicates many characteristic features of human asthma, this study evaluated the effects of treatment with anti-inflammatory drugs on the lesions of chronic asthma, and investigated potential underlying molecular mechanisms. Treatment with dexamethasone, a glucocorticoid, was compared with roflumilast, a novel phosphodiesterase-4 (PDE4) inhibitor. BALB/c mice sensitised to ovalbumin were challenged with a low mass concentration of aerosolised antigen for 30 min/day, 3 days/week for 6 weeks. In weeks 5 and 6, groups of animals were treated with either dexamethasone or roflumilast. Assessment included changes in acute-on-chronic inflammation, structural remodelling of the airways and airway hyper-responsiveness to a bronchoconstrictor stimulus. These were correlated with the expression of pro-inflammatory cytokines and growth factors. Compared to vehicle-treated control animals, dexamethasone- and roflumilast-treated mice exhibited reduced accumulation of intra-epithelial eosinophils and chronic inflammatory cells, including CD3+ T-lymphocytes in the airways. Similarly, both drugs inhibited subepithelial fibrosis and airway epithelial thickening, although only dexamethasone inhibited goblet cell hyperplasia/metaplasia. Airway hyper-reactivity was not diminished by either drug. Both treatments suppressed production of Th2 cytokines by ovalbumin-restimulated peribronchial lymph node cells. In selectively dissected airway tissue from vehicletreated animals, increased expression of mRNA for several pro-inflammatory cytokines (TNF-α, GM-CSF, IL-6) and cytokines characteristic of Th1 (IFN-γ), Th2 (IL-5, IL-13)and Th17 (IL-17A) cells was demonstrated using real-time PCR. Enhanced expression of growth factors (TGF-β1 and FGF-2) was also demonstrated in airway epithelium isolated by laser capture microdissection. Interestingly, whereas treatment with dexamethasone significantly inhibited expression of mRNA for all of the inflammationrelated cytokines examined, roflumilast inhibited only IL-17A, TNF-α, GM-CSF and IL-6. Both drugs inhibited mRNA expression of growth factors by epithelial cells. Because roflumilast was as effective as dexamethasone in suppressing inflammation and most changes of remodelling, the selective suppression of IL-17A, TNF-α, GM-CSF and IL-6 suggests that these mediators, or the cells that produce them, may have critical roles in pathogenesis. Furthermore, they may be particularly appropriate therapeutic targets in chronic asthma.
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Wu, Cheng-Kuan, and 胡靜君. "Inhalation Toxicity of Silver Nanoparticles in a Murine Model of Allergic Asthma." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/77311361258258222393.
Testo completoAbstract (sommario):
碩士<br>國立臺灣大學<br>環境衛生研究所<br>101<br>Nowadays, asthma is one of the most common airway inflammatory disease and its prevalence is high in developed and developing countries. A wide range of silver nanoparticle applications has emerged in consumer products ranging from disinfecting medical devices to water treatment. We are interested in the inhalation toxicity of silver nanoparticles in susceptible allergic asthmatic mice.
In this study, silver nanoparticles were produced in a generation system. The BALB/c mice were divided into normal group (PBS) and asthmatic group (induced by OVA injection). These two groups were further exposed for filtered air (FA) (PBS/FA (N=5)、OVA/FA (N=5)) and silver nanoparticles (NP) (PBS/NP (N=6)、OVA/NP (N=5)) 6 hours a day for one week.
The average size and concentration of NP during exposure was 32.78 nm at 3.34 mg/m3. The inflammation and asthma markers including IgE in serum, IL-13, total protein, total cells, proportion of neutrophils, macrophages and eosinophils in bronchoalveolar lavage fluid (BALF) and AHR (airway hyperresponsiveness) were determined.
The results showed that animals had adverse health effects after exposure to AgNPs (silver nanoparticles). In normal group, percentage of neutrophils, eosinophils and total cells in BALF increased after AgNPs exposure as compared to FA control. In asthma group, IgE, IL-13, AHR and total cells also increased after AgNPs exposure as compared to FA control but it was not statistically significant. These results suggested that asthmatic model needs further modification. Additionally, some previous experiments showed that AgNPs might act as anti-inflammatory agents. Thus，further studies are needed to assess the toxicity of AgNPs in allergic asthma model.
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Chen, Shew-Dan, and 陳秀丹. "Acute effect of methylprednisolone on brain in a rat model of asthma." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/69451809938767052212.
Testo completoAbstract (sommario):
碩士<br>國立陽明大學<br>急重症醫學研究所<br>96<br>Abstract
Asthma affects not only the airways but also the central nervous system (CNS). Corticosteroids are effective therapeutic agents for asthma. In our study, we investigated the acute effect of ovalbumin (OVA) on the brain and the effectiveness of methylprednisolone (MP) in both the periphery and CNS in a rat model of allergic asthma. Rats sensitized to OVA and exposed to OVA aerosol challenge to induce allergic asthma were compared with control rats and rats sensitized to OVA and pretreated with MP before OVA exposure. In response to OVA stimulation, the amount of c-Fos and glial fibrillary acidic protein (GFAP) increased, while that of neuronal nitric oxide synthase (nNOS) decreased in the nucleus tractus solitarius (NTS). In addition, the c-Fos, GFAP, and nNOS levels in the hippocampus and the nNOS levels in the olfactory bulb increased. However,the expression of these proteins in the frontal and cerebellar cortices was not affected by OVA stimulation. In contrast,pretreatment with MP before OVA exposure decreased the protein expression of c-Fos in the CA1 area, GFAP in NTS, and nNOS in CA1 and olfactory bulb, and while it increased the nNOS content in the NTS. These findings suggest that the brain responds to OVA stimulation in a rat model of allergic asthma and that MP treatment can not only ameliorate airway inflammation but also OVA-induced effects.
Keywords: asthma; brain; methylprednisolone; ovalbumin