Готові списки джерел за темами / Asthma model

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Добірка наукової літератури з теми "Asthma model"

Автор: Grafiati
Опубліковано: 25 січня 2025

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Статті в журналах з теми "Asthma model"

1

Tarlo, Susan M. "Occupational asthma: a valid model for adult asthma?" Current Opinion in Allergy and Clinical Immunology 3, no. 2 (April 2003): 91–94. http://dx.doi.org/10.1097/00130832-200304000-00001.

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2

Betters, R. Zachary, Robinder Khemani, and Patrick Ross. "1014: ASTHMA PREDICTION MODEL." Critical Care Medicine 44, no. 12 (December 2016): 329. http://dx.doi.org/10.1097/01.ccm.0000509690.21190.69.

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3

Zimmerman, Barry J., Sebastian Bonner, David Evans, and Robert B. Mellins. "Self-Regulating Childhood Asthma: A Developmental Model of Family Change." Health Education & Behavior 26, no. 1 (February 1999): 55–71. http://dx.doi.org/10.1177/109019819902600106.

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This article tests a model of self-regulatory development in which families’cognitive beliefs and behavioral skills for managing asthma symptoms emerge in four successive phases: asthma symptom avoidance, asthma acceptance, asthma compliance, and asthma self-regulation. Confirmatory factor analyses revealed that the hypothesized multiphase model provided the best factorial fit for phase items. Subsequent Guttman analyses of the families’phase scores revealed a high degree of sequential ordering. Finally, trend analyses of family phase differences revealed a significant negative linear relation with measures of asthma severity and a significant positive linear relation with physician care and concern measures, asthma regulatory measures, and beliefs in Western biomedical practices. Despite receiving primary care for asthma at a major metropolitan university hospital, 83% of the sample were classified as precompliant. The phase model of asthma self-regulatory development offers a qualitative approach for investigating the psychological determinants of asthma self-regulatory behavior.
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4

Creer, Thomas L., Ruth E. K. Stein, Leonard Rappaport, and Charles Lewis. "Behavioral Consequences of Illness: Childhood Asthma as a Model." Pediatrics 90, no. 5 (November 1, 1992): 808–15. http://dx.doi.org/10.1542/peds.90.5.808.

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Several areas of research on childhood asthma are discussed within a transactional model of asthma. The model emphasizes the multidirectional influences that affect the severity of asthma and associated behavioral disability. The initial focus is on how the clinical presentation and morbidity of asthma are affected both by somatic predisposition and by interactions with multiple internal and external elements. Specific elements include emotional factors, neuroimmunology, temperament, and medication side effects. Second, the impact of asthma on the child, his or her family, and segments of the community are described, as are consequences of the disorder on quality of life. Third, there is a synopsis of preventative interventions for reducing the medical and behavioral impact of childhood asthma. The motif is that the interaction of medical and behavioral procedures can improve the management of asthma while consequences of the disorder are mollified. Finally, as examples of a transactional model of asthma, selfmanagement programs for teaching children to become partners with their physicians in establishing and maintaining control over the disorder are described. A representative of self-management—the ACT (Asthma Care Training) program—is described, along with the impact such programs have on children, their families, and institutions. The conclusion emphasizes that asthma is a complicated and unpredictable disorder that puzzles physicians, behavioral scientists, and patients. Although new treatments may be over the horizon, controlling childhood asthma and its consequences currently rests on the cooperation and increased interaction of medical and behavioral scientists
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5

Ajami, Hicham, Hamid Mcheick, and Catherine Laprise. "First Steps of Asthma Management with a Personalized Ontology Model." Future Internet 14, no. 7 (June 22, 2022): 190. http://dx.doi.org/10.3390/fi14070190.

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Asthma is a chronic respiratory disease characterized by severe inflammation of the bronchial mucosa. Allergic asthma is the most common form of this health issue. Asthma is classified into allergic and non-allergic asthma, and it can be triggered by several factors such as indoor and outdoor allergens, air pollution, weather conditions, tobacco smoke, and food allergens, as well as other factors. Asthma symptoms differ in their frequency and severity since each patient reacts differently to these triggers. Formal knowledge is selected as one of the most promising solutions to deal with these challenges. This paper presents a new personalized approach to manage asthma. An ontology-driven model supported by Semantic Web Rule Language (SWRL) medical rules is proposed to provide personalized care for an asthma patient by identifying the risk factors and the development of possible exacerbations.
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6

Punyadasa, Dhanusha, Vindya Kumarapeli, and Wijith Senaratne. "Prevalence of being ‘high-risk’ of hospitalization due to exacerbation among asthma patients aged ≥ 20 years in a district of Sri Lanka." Journal of the College of Community Physicians of Sri Lanka 30, no. 2 (July 26, 2024): 133–42. http://dx.doi.org/10.4038/jccpsl.v30i2.8670.

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Introduction: Hospitalizations due to exacerbated asthma remai ns high in Sri Lanka leaving a huge burden on the healthcare system. Identification of the burden of ‘high risk asthma patients’ for hospitalization due to exacerbation is a cost-effective strategy for prioritizing management options. Objectives: To estimate the prevalence of ‘high-risk asthma patients ’ and selected risk predictors for hospitalization due to exacerbation among asthma patients aged ≥20 years in the district of Gampaha, Sri Lanka Methods: A community-based descriptive cross-sectional study was conducted among 1200 asthma patients aged ≥20 years, selected using a multistage sampling technique. The risk for hospi talization was assessed using a newly developed and validated risk prediction model. High-risk asthma patients were defi ned according to the cut-off value of the summary risk score of the model. Results: The prevalence of ‘high-risk asthma patients’ for hospitali zation due to exacerbation was 16.4% (95% CI: 14.2, 18.6). The prevalence of selected risk predictors: age ≥ 60 years 24.2% (95% CI: 21.9, 26.7), poor educational attainment 67.3% (95% CI: 64.5, 70.0), having diabetes mellitus 18.8% (95% CI: 16.5, 21.0), family history of asthma 41.3% (95% CI: 38.5, 44.2), ever smoked 12.2% (95% CI: 10.2, 14.1), ever int ubated or given intensive care 2.8% (95% CI: 1.8, 3.7), previous hospitalizations due to exacerbations 6.6% (95% CI: 5.1, 8.0) , having uncontrolled asthma 63.6% (95% CI: 60.8, 66.7), having symptomatic GORD 18% (95% CI: 15.7, 20.2) and ha ving body mass index (BMI) ≥ 25 kg/m2 36.3% (95% CI: 33.5, 39.0). Conclusions & Recommendations: A significant proportion of asthm a patients being at risk of hospitalization indicates the need to adopt cost-effective asthma management strategies to ac hieve better control of the disease. Prompt primary healthcare interventions are required to address modifiable risk predi ctors among asthma patients.
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7

Marshall, H. "New model of asthma proposed." Trends in Immunology 22, no. 4 (April 2001): 184. http://dx.doi.org/10.1016/s1471-4906(01)01913-5.

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8

Beggs, Paul John, and Peter Hayden Curson. "An Integrated Environmental Asthma Model." Archives of Environmental Health: An International Journal 50, no. 2 (April 1995): 87–94. http://dx.doi.org/10.1080/00039896.1995.9940884.

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9

Moldobaeva, Aigul, John Jenkins, Qiong Zhong, and Elizabeth M. Wagner. "Lymphangiogenesis in rat asthma model." Angiogenesis 20, no. 1 (October 27, 2016): 73–84. http://dx.doi.org/10.1007/s10456-016-9529-2.

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Park, Choon-Sik. "Role of Murine Asthma Model in Discovering Asthma Susceptible Genes." Allergy, Asthma & Immunology Research 6, no. 6 (2014): 475. http://dx.doi.org/10.4168/aair.2014.6.6.475.

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Дисертації з теми "Asthma model"

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.

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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.
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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.

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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.
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.
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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.

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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.

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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.

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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.

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Thesis (M.S.)--University of Missouri-Columbia, 2009.
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.
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Книги з теми "Asthma model"

1

Underwood, Stephen L. Studies on the mechanisms of pulmonary inflammation and airway hyperreactivity in animal models of asthma. London: University of East London, 1997.

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2

1953-, Raeburn D., and Giembycz M. A. 1961-, eds. Airways smooth muscle: Modelling the asthmatic response in vivo. Basel: Birkhäuser Verlag, 1996.

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3

Vanoirbeek, Jeroen. A Mouse Model For Chemical-Induced Asthma. Leuven Univ Pr, 2004.

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4

The Role of Cytokines in a Mouse Model of Allergic Asthma. CIP-GEGEVENS, HAAG, 1997.

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5

Hayes, James P. An experimental model of occupational asthma due to a low molecular weight chemical. 1992.

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6

Sj�bring, U., and J. D. Taylor, eds. Models of Exacerbations in Asthma and COPD. S. Karger AG, 2007. http://dx.doi.org/10.1159/isbn.978-3-8055-8173-8.

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7

Vithoulkas, George. A New Model of Health and Disease: Suggesting an Explanation for the Explosion of: AIDS, Cancer, Asthma, Candida, Epilepsy, Alzheimer's, Tuberculosis, Schizophrenia, Multiple Sclerosis, Allergic Conditions, Rheumatoid Arthritis, Chronic Fatigue Syndrome. North Atlantic Books, 1995.

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8

Costello, Richard Wilfred Kieran. Recruitment of eosinophils to airway nerves in asthma and in animal models of hyperractivity. 1997.

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A New Model of Health and Disease: Suggesting an Explanation for the Explosion of: AIDS, Cancer, Asthma, Candida, Epilepsy, Alzheimer's, Tuberculosis, Schizophrenia, Multiple Sclerosis, Allergic Conditions, Rheumatoid Arthritis, Chronic Fatigue Syndrome. International Academy of Classical Homeopathy Center of Homeopathic Medicine S.A., 2008.

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10

Strain, James J., and Michael Blumenfield, eds. Depression as a Systemic Illness. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603342.001.0001.

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Depression has been declared by the World Health Organization in March of 2017 to be the illness with the greatest burden of disease in the world. This volume attempts to examine the current state of our understanding of depressive disorders, from the animal models, allostatie load, patterns of recurrence, effects on other illnesses, for example, cancer, neurological, cardiovascular, wound healing, etc. It is from this perspective that the editors declare that depression is a systemic illness, not just a mental disorder. Therefore, primary care physicians need to know how to diagnose, treat, and refer when necessary for the non-complicated, non-refractory forms of depression. From this perspective models of mental health training for the primary care physician are reviewed. Then a new model, the medical model, a step beyond collaborative care is described. Non complicated depressive illness needs to be addressed by the primary care physician much as they do asthma, diabetes, hyptertension, and congestive heart failure. Even collaborative care models are unable as the number of psychiatrists is too few even in developed countries, let alone in developing ones to work with primary care. Medical schools and residency training programs need to incorporate curriculum and clinical experiences to accommodate developing expertise to diagnose, treat, and refer when necessary in this most common medical malady. Finally, a modified electronic medical record is proposed as a collaborating agent for the primary care physician.
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Частини книг з теми "Asthma model"

1

Winn, John Michael, Christopher M. Bishop, Thomas Diethe, John Guiver, and Yordan Zaykov. "Understanding asthma." In Model-Based Machine Learning, 303–54. Boca Raton: Chapman and Hall/CRC, 2023. http://dx.doi.org/10.1201/9780429192685-8.

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2

Franova, S., M. Joskova, V. Sadlonova, D. Pavelcikova, L. Mesarosova, E. Novakova, and M. Sutovska. "Experimental Model of Allergic Asthma." In Advances in Experimental Medicine and Biology, 49–55. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4549-0_7.

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3

Pauwels, R., G. Joos, and J. Kips. "The Rat as Experimental Model of Airway Hyperresponsiveness." In New Concepts in Asthma, 27–35. London: Macmillan Education UK, 1993. http://dx.doi.org/10.1007/978-1-349-12673-6_3.

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4

Tomkinson, Adrian. "The Sensitized Pig Model of Asthma." In Airways Smooth Muscle: Modelling the Asthmatic Response In Vivo, 225–40. Basel: Birkhäuser Basel, 1996. http://dx.doi.org/10.1007/978-3-0348-9000-7_10.

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Daubeuf, F., and Nelly Frossard. "Eosinophils and the Ovalbumin Mouse Model of Asthma." In Methods in Molecular Biology, 283–93. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1016-8_24.

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Royer, Christopher, Lisa A. Miller, and Angela Haczku. "A Novel Nonhuman Primate Model of Nonatopic Asthma." In Methods in Molecular Biology, 83–94. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2364-0_6.

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Chan-Yeung, Moira. "Occupational Asthma — A Model to Study the Natural History and Pathogenic Mechanisms in Asthma." In New Drugs in Allergy and Asthma, 107–18. Basel: Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-7324-6_9.

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8

Roeder, Thomas, Kerstin Isermann, Christina Wagner, and Christine Warmbold. "Fruit Flies as Models in Biomedical Research – A Drosophila Asthma Model." In Insect Biotechnology, 15–27. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9641-8_2.

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9

Choi, Jongmyung, Hee Young Jeong, and Rosa I. Arriaga. "A Ubiquitous Community Care Model for Pediatric Asthma Patients." In Human Centric Technology and Service in Smart Space, 137–44. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-5086-9_18.

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10

Gauvreau, Gail M., and Michelle Y. Evans. "Allergen Inhalation Challenge: A Human Model of Asthma Exacerbation." In Contributions to Microbiology, 21–32. Basel: KARGER, 2007. http://dx.doi.org/10.1159/000107052.

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Тези доповідей конференцій з теми "Asthma model"

1

Henshaw, Ekpo Raphael, Victor Chukwudi Osamor, and Ambrose A. Azeta. "Federated Learning-Based Asthma Prediction Model in Children." In 2024 International Conference on Science, Engineering and Business for Driving Sustainable Development Goals (SEB4SDG), 1–6. IEEE, 2024. http://dx.doi.org/10.1109/seb4sdg60871.2024.10629888.

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Tokunaga, Yosihisa, Haruki Imaoka, Yoshitaka Morimatsu, Yoichiro Kaku, Yuki Sakazaki, Masanobu Matsuoka, Yoshihiro Komohara, Tomotaka Kawayama, Motohiro Takeya, and Tomoaki Hoshino. "Role of CD163 in human fatal asthma and murine asthma model." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa648.

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3

Bamashmoos, Fatmah, and Theo Tryfonas. "Towards Asthma Self-Management: An Integrated Ontology Model for Asthma Action Plan." In 2019 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2019. http://dx.doi.org/10.1109/bibm47256.2019.8983363.

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4

Shahabi, Shahram, Ebrahim Mazloomi, Behrooz Ilkhanizadeh, and Ahad Zare. "Subcutaneous Isopathic Immunotherapy of Allergic Asthma in a Mouse Model of Allergic Asthma." In HRI London 2019—Cutting Edge Research in Homeopathy: Presentation Abstracts. The Faculty of Homeopathy, 2020. http://dx.doi.org/10.1055/s-0040-1702082.

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5

Carpaij, Orestes, Judith Vonk, Martijn Nawijn, Huib Kerstjens, Gerard Koppelman, and Maarten Van Den Berge. "Externally validating the asthma remission prediction model to the Dutch asthma remission studies." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa4512.

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6

Pushpalatha, M. P., and M. R. Pooja. "A predictive model for the effective prognosis of Asthma using Asthma severity indicators." In 2017 International Conference on Computer Communication and Informatics (ICCCI). IEEE, 2017. http://dx.doi.org/10.1109/iccci.2017.8117717.

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Rhee, Chin Kook, Jee Hye Kim, Shin Young Kim, Chan Kwon Park, and Hyoung Kyu Yoon. "Effect of roflumilast on neutrophilic asthma model." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa1147.

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8

Zeng, Zhimin, Fengjia Chen, and Yubiao Guo. "An Asthma-COPD Overlap Mouse Model Establishment." In ERS Congress 2024 abstracts, PA433. European Respiratory Society, 2024. http://dx.doi.org/10.1183/13993003.congress-2024.pa433.

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9

Oros, M., A. Manda, C. Codleanu, L. Calapod, C. Radu, R. Bogdan, E. Bulacu, et al. "Medical Home for Asthma: A New Model for Childhood Asthma Management in Primary Care." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4803.

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10

Brandao-Rangel, Maysa A. R., Renilson Moraes-Ferreira, Anamei Silva-Reis, Victor Hugo Souza Palmeira, Francine Maria Almeida, Fabiana Regina Da Silva Olimpio, Flavio Aimbire, et al. "Aerobic Exercise Improves Asthma Phenotype in a Model of Severe Asthma: Involvement of Kinins." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa2328.

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Звіти організацій з теми "Asthma model"

1

Collie, D. D., J. A. Wilder, and D. E. Bice. Nonspecific airway reactivity in a mouse model of asthma. Office of Scientific and Technical Information (OSTI), December 1995. http://dx.doi.org/10.2172/381396.

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2

E, Flemyng, and Mitchell D. Increased versus stable doses of inhaled steroids for exacerbations of chronic asthma in adults and children: Protocol. Epistemonikos Interactive Evidence Synthesis, January 2022. http://dx.doi.org/10.30846/ies.b984bf9656.v3.

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Анотація:
Abstract Rationale Early treatment of asthma exacerbations with inhaled corticosteroids is the best strategy for management, although use of an increased or stable dose is questioned. Objectives To compare the clinical effectiveness and safety of increased versus stable doses of inhaled corticosteroids as part of a patient-initiated action plan for the home management of exacerbations in children and adults with persistent asthma. Search methods We searched the Cochrane Airways Group Specialised Register (part of CENTRAL), MEDLINE, Embase, CINAHL, major trials registries and handsearched abstracts up to 20 December 2021. Eligibility criteria Parallel and cross-over blinded randomised controlled trials (RCTs) Outcomes Treatment failure (the need for rescue oral steroids) in the randomised population and in the subset who initiated the study inhaler, unscheduled physician visits, unscheduled acute care, emergency department or hospital visits, serious and non-serious adverse events, and duration of exacerbation. Risk of bias We used Risk of Bias 2 (RoB 2)and the tool's extension for cross-over trials. Synthesis methods We conducted meta-analyses using fixed-effect models to calculate odds ratios (OR) and 95% confidence intervals (CI) for all but one outcome, which used random-effects models due to heterogeneity (treatment failure in the subset who initiated the study inhaler). We summarised certainty of evidence according to GRADE methods. Included studies We included nine RCTs (seven parallel and two cross‐over) with a total of 1923 participants. The studies were conducted in Europe, North America, and Australasia and were published between 1998 and 2018. Five studies evaluated adult populations (1247 participants; ≥ 15 years), and four studies evaluated child or adolescent populations (676 participants; < 15 years). Approximately 50% of randomised participants initiated the study inhaler (range 23% to 100%). The studies reported treatment failure in various ways, so we made assumptions to allow us to combine data. Synthesis of results People randomised to increase their inhaled corticosteroids dose at the first signs of an exacerbation probably had similar odds of needing rescue oral corticosteroids to those randomised to a placebo inhaler (OR 0.97, 95% CI 0.76 to 1.25; 8 studies, 1774 participants; moderate-certainty evidence). Results for the same outcome in the subset of participants who initiated the study inhaler (approximately 50%) gives a different point estimate with very low certainty due to heterogeneity, imprecision and risk of bias (OR 0.84, 95% CI 0.54 to 1.30; 7 studies, 766 participants; random-effects model used). For adverse effects, imprecision and risk of bias from missing data, outcome measurement and reporting meant we were very uncertain about the effect estimate (serious adverse events OR 1.69, 95% CI 0.77 to 3.71; 2 studies, 394 participants; non-serious adverse events OR 2.15, 95% CI 0.68 to 6.73; 2 studies, 142 participants). We had very low confidence in the effect estimates for unscheduled physician visits, unscheduled acute care, emergency department or hospital visits and duration of exacerbation due to risk of bias. Authors' conclusions Evidence suggests that adults and children with mild to moderate asthma are unlikely to have an important reduction in the need for oral steroids from increasing a patient's inhaled corticosteroid dose at the first sign of an exacerbation. Other clinically important benefits and potential harms cannot be ruled out due to wide confidence intervals, risk of bias in the studies, and assumptions made for synthesis when combining data. Included studies reflect evolving clinical practice and study methods, and the data do not support thorough investigation of effect modifiers such as baseline dose, fold increase, asthma severity and timing. The review does not include recent evidence from pragmatic, unblinded studies showing benefits of larger dose increases in those with poorly controlled asthma. Differences between the blinded and unblinded studies should be investigated. Funding This Cochrane Review had no dedicated funding. Registration Protocol (2009): doi.org/10.1002/14651858.CD007524 Original review (2010): doi.org/10.1002/14651858.CD007524.pub3 Review update (2014): doi.org/10.1002/14651858.CD007524.pub4
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3

E, Flemyng, and Mitchell D. Increased versus stable doses of inhaled steroids for exacerbations of chronic asthma in adults and children: Protocol. Epistemonikos Interactive Evidence Synthesis, January 2022. http://dx.doi.org/10.30846/ies.b984bf9699.v2.

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Анотація:
Abstract Rationale Early treatment of asthma exacerbations with inhaled corticosteroids is the best strategy for management, although use of an increased or stable dose is questioned. Objectives To compare the clinical effectiveness and safety of increased versus stable doses of inhaled corticosteroids as part of a patient-initiated action plan for the home management of exacerbations in children and adults with persistent asthma. Search methods We searched the Cochrane Airways Group Specialised Register (part of CENTRAL), MEDLINE, Embase, CINAHL, major trials registries and handsearched abstracts up to 20 December 2021. Eligibility criteria Parallel and cross-over blinded randomised controlled trials (RCTs) Outcomes Treatment failure (the need for rescue oral steroids) in the randomised population and in the subset who initiated the study inhaler, unscheduled physician visits, unscheduled acute care, emergency department or hospital visits, serious and non-serious adverse events, and duration of exacerbation. Risk of bias We used Risk of Bias 2 (RoB 2)and the tool's extension for cross-over trials. Synthesis methods We conducted meta-analyses using fixed-effect models to calculate odds ratios (OR) and 95% confidence intervals (CI) for all but one outcome, which used random-effects models due to heterogeneity (treatment failure in the subset who initiated the study inhaler). We summarised certainty of evidence according to GRADE methods. Included studies We included nine RCTs (seven parallel and two cross‐over) with a total of 1923 participants. The studies were conducted in Europe, North America, and Australasia and were published between 1998 and 2018. Five studies evaluated adult populations (1247 participants; ≥ 15 years), and four studies evaluated child or adolescent populations (676 participants; < 15 years). Approximately 50% of randomised participants initiated the study inhaler (range 23% to 100%). The studies reported treatment failure in various ways, so we made assumptions to allow us to combine data. Synthesis of results People randomised to increase their inhaled corticosteroids dose at the first signs of an exacerbation probably had similar odds of needing rescue oral corticosteroids to those randomised to a placebo inhaler (OR 0.97, 95% CI 0.76 to 1.25; 8 studies, 1774 participants; moderate-certainty evidence). Results for the same outcome in the subset of participants who initiated the study inhaler (approximately 50%) gives a different point estimate with very low certainty due to heterogeneity, imprecision and risk of bias (OR 0.84, 95% CI 0.54 to 1.30; 7 studies, 766 participants; random-effects model used). For adverse effects, imprecision and risk of bias from missing data, outcome measurement and reporting meant we were very uncertain about the effect estimate (serious adverse events OR 1.69, 95% CI 0.77 to 3.71; 2 studies, 394 participants; non-serious adverse events OR 2.15, 95% CI 0.68 to 6.73; 2 studies, 142 participants). We had very low confidence in the effect estimates for unscheduled physician visits, unscheduled acute care, emergency department or hospital visits and duration of exacerbation due to risk of bias. Authors' conclusions Evidence suggests that adults and children with mild to moderate asthma are unlikely to have an important reduction in the need for oral steroids from increasing a patient's inhaled corticosteroid dose at the first sign of an exacerbation. Other clinically important benefits and potential harms cannot be ruled out due to wide confidence intervals, risk of bias in the studies, and assumptions made for synthesis when combining data. Included studies reflect evolving clinical practice and study methods, and the data do not support thorough investigation of effect modifiers such as baseline dose, fold increase, asthma severity and timing. The review does not include recent evidence from pragmatic, unblinded studies showing benefits of larger dose increases in those with poorly controlled asthma. Differences between the blinded and unblinded studies should be investigated. Funding This Cochrane Review had no dedicated funding. Registration Protocol (2009): doi.org/10.1002/14651858.CD007524 Original review (2010): doi.org/10.1002/14651858.CD007524.pub3 Review update (2014): doi.org/10.1002/14651858.CD007524.pub4
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4

E, Flemyng, and Mitchell D. Increased versus stable doses of inhaled steroids for exacerbations of chronic asthma in adults and children: Update. Epistemonikos Interactive Evidence Synthesis, January 2022. http://dx.doi.org/10.30846/ies.b984bf9639.v2.

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Анотація:
Abstract Rationale Early treatment of asthma exacerbations with inhaled corticosteroids is the best strategy for management, although use of an increased or stable dose is questioned. Objectives To compare the clinical effectiveness and safety of increased versus stable doses of inhaled corticosteroids as part of a patient-initiated action plan for the home management of exacerbations in children and adults with persistent asthma. Search methods We searched the Cochrane Airways Group Specialised Register (part of CENTRAL), MEDLINE, Embase, CINAHL, major trials registries and handsearched abstracts up to 20 December 2021. Eligibility criteria Parallel and cross-over blinded randomised controlled trials (RCTs) Outcomes Treatment failure (the need for rescue oral steroids) in the randomised population and in the subset who initiated the study inhaler, unscheduled physician visits, unscheduled acute care, emergency department or hospital visits, serious and non-serious adverse events, and duration of exacerbation. Risk of bias We used Risk of Bias 2 (RoB 2)and the tool's extension for cross-over trials. Synthesis methods We conducted meta-analyses using fixed-effect models to calculate odds ratios (OR) and 95% confidence intervals (CI) for all but one outcome, which used random-effects models due to heterogeneity (treatment failure in the subset who initiated the study inhaler). We summarised certainty of evidence according to GRADE methods. Included studies We included nine RCTs (seven parallel and two cross‐over) with a total of 1923 participants. The studies were conducted in Europe, North America, and Australasia and were published between 1998 and 2018. Five studies evaluated adult populations (1247 participants; ≥ 15 years), and four studies evaluated child or adolescent populations (676 participants; < 15 years). Approximately 50% of randomised participants initiated the study inhaler (range 23% to 100%). The studies reported treatment failure in various ways, so we made assumptions to allow us to combine data. Synthesis of results People randomised to increase their inhaled corticosteroids dose at the first signs of an exacerbation probably had similar odds of needing rescue oral corticosteroids to those randomised to a placebo inhaler (OR 0.97, 95% CI 0.76 to 1.25; 8 studies, 1774 participants; moderate-certainty evidence). Results for the same outcome in the subset of participants who initiated the study inhaler (approximately 50%) gives a different point estimate with very low certainty due to heterogeneity, imprecision and risk of bias (OR 0.84, 95% CI 0.54 to 1.30; 7 studies, 766 participants; random-effects model used). For adverse effects, imprecision and risk of bias from missing data, outcome measurement and reporting meant we were very uncertain about the effect estimate (serious adverse events OR 1.69, 95% CI 0.77 to 3.71; 2 studies, 394 participants; non-serious adverse events OR 2.15, 95% CI 0.68 to 6.73; 2 studies, 142 participants). We had very low confidence in the effect estimates for unscheduled physician visits, unscheduled acute care, emergency department or hospital visits and duration of exacerbation due to risk of bias. Authors' conclusions Evidence suggests that adults and children with mild to moderate asthma are unlikely to have an important reduction in the need for oral steroids from increasing a patient's inhaled corticosteroid dose at the first sign of an exacerbation. Other clinically important benefits and potential harms cannot be ruled out due to wide confidence intervals, risk of bias in the studies, and assumptions made for synthesis when combining data. Included studies reflect evolving clinical practice and study methods, and the data do not support thorough investigation of effect modifiers such as baseline dose, fold increase, asthma severity and timing. The review does not include recent evidence from pragmatic, unblinded studies showing benefits of larger dose increases in those with poorly controlled asthma. Differences between the blinded and unblinded studies should be investigated. Funding This Cochrane Review had no dedicated funding. Registration Protocol (2009): doi.org/10.1002/14651858.CD007524 Original review (2010): doi.org/10.1002/14651858.CD007524.pub3 Review update (2014): doi.org/10.1002/14651858.CD007524.pub4
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5

E, Flemyng, and Mitchell D. Increased versus stable doses of inhaled steroids for exacerbations of chronic asthma in adults and children: Protocol. Epistemonikos Interactive Evidence Synthesis, January 2022. http://dx.doi.org/10.30846/ies.b984bf9656.v2.

Повний текст джерела
Анотація:
Abstract Rationale Early treatment of asthma exacerbations with inhaled corticosteroids is the best strategy for management, although use of an increased or stable dose is questioned. Objectives To compare the clinical effectiveness and safety of increased versus stable doses of inhaled corticosteroids as part of a patient-initiated action plan for the home management of exacerbations in children and adults with persistent asthma. Search methods We searched the Cochrane Airways Group Specialised Register (part of CENTRAL), MEDLINE, Embase, CINAHL, major trials registries and handsearched abstracts up to 20 December 2021. Eligibility criteria Parallel and cross-over blinded randomised controlled trials (RCTs) Outcomes Treatment failure (the need for rescue oral steroids) in the randomised population and in the subset who initiated the study inhaler, unscheduled physician visits, unscheduled acute care, emergency department or hospital visits, serious and non-serious adverse events, and duration of exacerbation. Risk of bias We used Risk of Bias 2 (RoB 2)and the tool's extension for cross-over trials. Synthesis methods We conducted meta-analyses using fixed-effect models to calculate odds ratios (OR) and 95% confidence intervals (CI) for all but one outcome, which used random-effects models due to heterogeneity (treatment failure in the subset who initiated the study inhaler). We summarised certainty of evidence according to GRADE methods. Included studies We included nine RCTs (seven parallel and two cross‐over) with a total of 1923 participants. The studies were conducted in Europe, North America, and Australasia and were published between 1998 and 2018. Five studies evaluated adult populations (1247 participants; ≥ 15 years), and four studies evaluated child or adolescent populations (676 participants; < 15 years). Approximately 50% of randomised participants initiated the study inhaler (range 23% to 100%). The studies reported treatment failure in various ways, so we made assumptions to allow us to combine data. Synthesis of results People randomised to increase their inhaled corticosteroids dose at the first signs of an exacerbation probably had similar odds of needing rescue oral corticosteroids to those randomised to a placebo inhaler (OR 0.97, 95% CI 0.76 to 1.25; 8 studies, 1774 participants; moderate-certainty evidence). Results for the same outcome in the subset of participants who initiated the study inhaler (approximately 50%) gives a different point estimate with very low certainty due to heterogeneity, imprecision and risk of bias (OR 0.84, 95% CI 0.54 to 1.30; 7 studies, 766 participants; random-effects model used). For adverse effects, imprecision and risk of bias from missing data, outcome measurement and reporting meant we were very uncertain about the effect estimate (serious adverse events OR 1.69, 95% CI 0.77 to 3.71; 2 studies, 394 participants; non-serious adverse events OR 2.15, 95% CI 0.68 to 6.73; 2 studies, 142 participants). We had very low confidence in the effect estimates for unscheduled physician visits, unscheduled acute care, emergency department or hospital visits and duration of exacerbation due to risk of bias. Authors' conclusions Evidence suggests that adults and children with mild to moderate asthma are unlikely to have an important reduction in the need for oral steroids from increasing a patient's inhaled corticosteroid dose at the first sign of an exacerbation. Other clinically important benefits and potential harms cannot be ruled out due to wide confidence intervals, risk of bias in the studies, and assumptions made for synthesis when combining data. Included studies reflect evolving clinical practice and study methods, and the data do not support thorough investigation of effect modifiers such as baseline dose, fold increase, asthma severity and timing. The review does not include recent evidence from pragmatic, unblinded studies showing benefits of larger dose increases in those with poorly controlled asthma. Differences between the blinded and unblinded studies should be investigated. Funding This Cochrane Review had no dedicated funding. Registration Protocol (2009): doi.org/10.1002/14651858.CD007524 Original review (2010): doi.org/10.1002/14651858.CD007524.pub3 Review update (2014): doi.org/10.1002/14651858.CD007524.pub4
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6

Hong, Zheng, Ying Liu, Hanyu Fang, Bang Yu, and Hongchun Zhang. Anti-inflammatory effects of Astragaloside IV in animal models of asthma: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2022. http://dx.doi.org/10.37766/inplasy2022.10.0014.

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7

Reuter, W. G., J. H. Underwood, and J. C. Newman. Review of ASTM Symposium on Surface Crack Growth: Models, Experiments, and Structures. Fort Belvoir, VA: Defense Technical Information Center, November 1990. http://dx.doi.org/10.21236/ada230645.

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8

Shannon. L51584 Effect of Water Chemistry on Internal Corrosion Rates in Offshore Pipelines.pdf. Chantilly, Virginia: Pipeline Research Council International, Inc. (PRCI), March 1988. http://dx.doi.org/10.55274/r0010643.

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This work is an extension of a program reported in 1984 to establish factors which control corrosion of API line pipe in gas containing carbon dioxide and water. In this phase of the program, there were four objectives. One was to establish the temperature of maximum corrosion in the range of 75�, 100� and 175�F at 1000 psi in water saturated with carbon dioxide at partial pressures of 15 and 50 psia. The next was to explore the role of carbon content and microstructure in the steel, iron carbonate film formation, and resulting corrosion rates. The third was to examine the role of pre-existing mill scale and corrosion films on accelerating pitting attack. The final objective was to extend a spread sheet computer model to calculate corrosion rates from field data. Tests were run in a refreshed, recirculating autoclave at a total pressure of 1000 psi in water saturated with CO2 at partial pressures of 15 and 50 psia, and containing bicarbonate ion to adjust the pH either to 5 or 6. Six materials were tested: ASTM-A53B, two lots of API5LX-X52 and three lots of API5LX-X60. Samples were pulled at intervals for weight loss corrosion and to examine the surface films by electron microscope and metallography. After plotting the weight loss results, corrosion rates in mils per year (MPY) were calculated. The microstructure of the metal, the corrosion films of iron carbonate, and the weight loss results were then examined. The corrosion data were incorporated into a spread sheet computer model for users to calculate their own pipe line corrosion rates.
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9

Shen, Gianetto, and Tyson. L52342 Development of Procedure for Low-Constraint Toughness Testing Using a Single-Specimen Technique. Chantilly, Virginia: Pipeline Research Council International, Inc. (PRCI), December 2011. http://dx.doi.org/10.55274/r0010687.

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Pipelines from remote frontier regions are increasingly required to have adequate resistance to large deformations such as that caused by ground movement. In response to this, �strain-based design"� has been developed to enable assessment of imperfections at applied strains beyond yield. In addition, it is proposed to take advantage of the increased apparent toughness of pipe under low constraint, such as girth weld imperfections under axial tension, compared with the high-constraint toughness measured in conventional tests such as ASTM E1290 [1]. Application of low-constraint testing has been dvantageously applied in assessment of toughness for offshore pipeline projects. Also in the pipeline industry, demands on new pipeline projects include low design temperatures as well as high strain capacity. At the same time, increased strength is specified, which increases the level of required toughness. These factors make it increasingly important to assure weldment toughness, in particular to ensure that the failure mode remains ductile. It is well known that brittle cleavage is especially sensitive to constraint, and the availability of a toughness test that would reproduce field conditions would enable more rational development and acceptance of candidate welds and, in particular, enable more appropriate testing of weld heat-affected zones. This work was performed for specific application to surface circumferential cracks in pipe under strain-based design, for which the best constraint matching has been found to occur for clamped single-edge tension (SE(T)) specimens with H/W=10. For this geometry, a test procedure similar to that of ASTM E1820-06 for single-edge bend (SE(B)) and compact tension (C(T)) specimens was developed for J-resistance tests using a single-specimen technique. All the equations used in the procedure, including those for evaluation of J-integrals from the area under load/plastic crack mouth opening displacement (CMOD) curves, and evaluation of crack length from unloading compliance including rotation correction, were developed using finite element analysis (FEA) with a range of crack depths, focusing on a/W= 0.2 to 0.5 which is of most practical interest. The present procedure is compared with that of E1820 for SE(B) testing regarding evaluation of J-integral with crack growth correction, crack length evaluation, and correction of compliance for rotation.
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10

Supported self-management for people with asthma is the most effective model of care. National Institute for Health Research, December 2020. http://dx.doi.org/10.3310/alert_43023.

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