Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute respiratory distress syndrome is a serious sequelae of many serious illnesses during pregnancy. An understanding of acute respiratory distress syndrome is central to the proper care of a patient with the disorder. Acute respiratory distress syndrome results in diminished pulmonary compliance and respiratory shunt mediated hypoxemia. Furthermore, the initial pulmonary injury in acute respiratory distress syndrome may be further worsened by therapeutic hyperoxia and barotrauma. Limitation of peak-plateau airway pressure to less than 35 to 40 cm H2O may reduce barotrauma. Inflammatory mediator therapy may hold future promise in attenuation of lung injury induced by acute respiratory distress syndrome. Aggressive care may help those pregnant patients afflicted with acute respiratory distress syndrome.
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PMID:Acute respiratory distress syndrome in pregnancy. 929 21

In this study, we examined the sequential expression of several matrix metalloproteinases (MMPs), tissue inhibitors of metalloproteinases (TIMPs), and growth factors as well as the presence of apoptosis in a model of pulmonary fibrosis induced in rats with paraquat and hyperoxia. Animals showing neither clinical nor morphological changes with this double aggression were classified as "resistant". Rats were killed at 1, 2, 3, and 6 wk, and lungs were used for collagen content, gene expression by real-time PCR, gelatinolytic activity by zymography, apoptosis by in situ DNA fragmentation, and protein localization by immunohistochemistry. Our results showed a significant decrease of collagenases MMP-8 and MMP-13, with an increase of TIMP-1 and transforming growth factor-beta. Immunoreactive TIMP-1 was increased in experimental rats and primarily localized in alveolar macrophages. Expression of gelatinases MMP-2 and MMP-9 mRNAs was not affected, but lung zymography revealed an increase in progelatinase B, progelatinase A, and its active form. Epithelial apoptosis was evident from the first week, whereas at later periods, interstitial cell apoptosis was also noticed. Resistant animals behave as controls. These findings suggest that an imbalance between collagenases and TIMPs, excessive gelatinolytic activity, and epithelial apoptosis participate in the fibrotic response in this experimental model.
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PMID:Unbalanced collagenases/TIMP-1 expression and epithelial apoptosis in experimental lung fibrosis. 1288 63