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Reversible and irreversible airway inflammation and fibrosis in mice exposed to inhaled ovalbumin 总被引:1,自引:0,他引:1
Objective and design: We examined the reversibility of several changes in the lungs and airways of mice immediately after exposure to ovalbumin aerosol and after a period of recovery breathing clean air.Methods: Mice were exposed for 1, 2, 4, 6, 8, or 10 weeks, with recovery in clean air for 1–3 weeks.Results: Airway collagen content, exhaled NO, airway mucous cell hyperplasia, and lung lavage inflammatory cell content increased upon exposure to ovalbumin aerosol. All parameters except airway fibrosis decreased partially or completely to control values with recovery in clean air.Conclusions: Airway mucous cell hypertrophy and hyperplasia appear to be completely reversible after recovery in clean air, while exhaled NO and airway inflammation appear to be mostly reversible, except for persistence of lymphocytes in the lung lavage fluid. Airway fibrosis appears to be reversible when mice are exposed to ovalbumin aerosol for periods of up to 4 weeks of exposure, but becomes irreversible after 6 or more weeks of exposure.Received 30 June 2004; returned for revision 24 September 2004; accepted by J. S. Skotnicki 13 October 2004 相似文献
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Abstract In this study, gingival crevicular fluid (GCF) was collected from around a canine tooth, in children, before and during orthodontic tooth movement. The aim was to identify and quantify the glycosaminoglycan (GAG) components of GCF and relate them to tooth movement, gingival inflammation, plaque accumulation, pocket probing depth and GCF volume recorded at the site of sampling. GAG in GCF samples, collected for a 15-min period into microcapillary tubes, were separated electrophoretically, stained with Alcian blue and quantified using a laser densitometer. 2 GAG components of hyaluronic acid (HA) and chondroitin sulphate (CS) were identified. The increase in GCF volume during orthodontic tooth movement was only partly due to increased gingival inflammation, GAG levels varied with different types of orthodontic tooth movement. In GCF, levels of CS, in particular, may reflect the changes in the deeper periodontal tissues which could be monitored during orthodontic tooth movements. 相似文献
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Early cellular events in pulmonary fibrosis 总被引:5,自引:0,他引:5
In this review we have surveyed recent investigations of early cellular events in pulmonary fibrosis both in animal models and in human diseases. Analysis of the interactions of the numerous cell types in the lung following injury is an almost overwhelmingly complex enterprise. In the animal models experimental design has a profound effect on results, making it difficult to compare studies when species, fibrogenic agent, dose, route of exposure, schedule of administration, time course, and analytical methods may not be equivalent. In human diseases we are rarely able to obtain data at precisely the same time point in the course of the disease even among patients in the same study, and possible confounding variables present are legion. Transcending these difficulties for the moment, can we draw any conclusions from our current knowledge of early cellular interactions in pulmonary fibrosis? What is striking is not that there are so many agents that can potentially induce pulmonary fibrosis, but that the lung has such capabilities for recovery. Although the major effector cells may all initially participate in damaging the lung and initiating fibrosis, there is evidence that they may also have the capacity to participate in subsequent repair. Macrophages may initially recruit fibroblasts and stimulate them to proliferate, only to suppress them subsequently. Macrophage production of prostaglandins can lead to suppression of macrophage, neutrophil and lymphocyte responses, thus attenuating tissue injury and the development of fibrosis. Neutrophils may initially release toxic metabolites and enzymes that damage parenchyma. However, there is evidence that they may later play a role in attenuating fibrosis, perhaps through collagenase secretion, or through as yet unknown mechanisms. Lymphocytes may initially participate in a number of damaging ways by secreting chemoattractants for other cells and participating in destructive autoimmune processes. However, there is evidence that subpopulations of T cells may dramatically shift during the course of fibrosis, leading to attenuation of the process. It may thus be useful to consider irreversible pulmonary fibrosis as the end result of a process in which the balance of normal injury/repair mechanisms is disrupted. There is clearly no single "fibrogenic event." Rather, there seem to be a number of places where disruption of balance/repair processes may begin. In diseases of unknown etiology such as sarcoidosis or IPF, loss of control may occur at the genetic level, leading to the destructive alveolitis that is the apparent precursor of fibrosis.(ABSTRACT TRUNCATED AT 400 WORDS) 相似文献
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C G Last C C Strauss 《Journal of the American Academy of Child and Adolescent Psychiatry》1990,29(1):31-35
The characteristics of anxiety-based school refusal were examined in 63 school refusing children and adolescents referred to an outpatient anxiety disorder clinic. Patients were assessed on sociodemographic, diagnostic, and personality variables, as well as familial history of school refusal. Results suggest that there are two primary diagnostic "subgroups" of school refusers--separation anxious and phobic. Phobic school refusers had a later age of onset and showed more pervasive (severe) school refusal than separation anxious school refusers. By contrast, separation anxious school refusers were more likely than phobic school refusers to have mothers who had a history of school refusal problems. The implications of these findings are discussed. 相似文献
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Julie Lynch Jason Last Philip Dodd Daniela Stancila Christine Linehan 《Disability and health journal》2019,12(1):65-71