Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of vitamin E deficiency on bleomycin (BLM)-induced pulmonary fibrosis have been studied by analyses of pressure volume (PV) curves and morphological examinations. Golden hamsters were divided into groups on a control diet (group C), vitamin E-deficient diet (E), control diet with BLM treatment (CB), and vitamin E-deficient diet with BLM treatment (EB). Group EB showed PV curves shifted downward and to the right soon after BLM administration (10 days) and gradually shifted upward and to the left compared to group CB in the later period (30 and 60 days after BLM treatment). Histologically group EB was characterized by relatively severe interstitial pneumonitis in the early stages. In later stages, emphysematous changes were induced in combination with a lesser degree of fibrosis in group EB. Mean thickness of the alveolar wall of group CB was larger than group C while that of group EB was smaller at 30 days after BLM treatment. These results indicate that, with BLM treatment, vitamin E-deficient hamsters show increased distensibility on the PV curve and emphysematous changes mixed with focal fibrosis on morphological examination. This means that by adding other modulating factors, such as vitamin E deficiency, BLM, an agent known to produce pulmonary fibrosis, acts to induce an emphysematous lesion in the lung. Although pulmonary fibrosis and emphysema have been considered to be final and different forms of parenchymal injury, each may proceed to the other under the influence of some modulating factors.
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PMID:Effects of vitamin E deficiency on bleomycin-induced pulmonary fibrosis in the hamster. 245 80

Some premature and mature newborns who require intermittent positive airway pressure (IPPV) and high oxygen concentrations for respiratory distress syndrome develop characteristic damage of bronchi and bronchioles termed broncho-pulmonary dysplasia (BPD). According to the radiographic findings the changes are categorized into four progressive stages. Stage 1 describes a radiographic feature with a pattern of fine, faint granularity as it is characteristic for the hyaline-membrane-syndrome. Stages 2 to 4 represent diffuse interstitial emphysema, a bubbly appearance of the lung, atelectasis and a progressive fibrosis. Electronmicroscopic investigations of bronchial imprints could demonstrate a rarefication of the cilia and a ciliary damage which took the form of compound cilia. In addition, a marked increase of goblet cells in the bronchial mucosa as well as a metaplasia of the epithelial cells was present. These findings may be a prerequisite for chronic infections, and perpetuate a cycle which may result in chronic obstructive airway disease. The significance of bronchial and bronchiolar injury in children with BPD is said to be due to IPPV, high inspiratory oxygen concentrations, high fluid intake, vitamin E deficiency or an increased intrapulmonary pressure secondary to a patent ductus arteriosus. When pulmonary mechanics were measured in a baby-body-plethysmograph a high pulmonary resistance and a low dynamic compliance occurred at the first investigation after IPPV or oxygen administration. On re-examination there was a strong tendency to normalisation of x-ray findings and pulmonary mechanics, depending upon the time which elapsed between ventilation and re-examination. Current therapy has to be symptomatic and may include secretolytics, glucocorticoids and bronchodilators. The preventive interventions have to take into consideration ventilation techniques, restrictions in O2 and fluid intake.
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PMID:[Pulmonary dysplasia in infancy. Pathogenesis, pneumologic course studies and therapy possibilities]. 647 97